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Minipress (Prazosin)

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Minipress is an effective strong preparation which is taken in treatment of hypertension diseases. Minipress is also helpful in treatment of male prostate enlargement symptoms, congestive heart failure, Raynaud's disease. Minipress acts as anti-hypertension remedy.

Other names for this medication:

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Also known as:  Prazosin.


Minipress is created by pharmacy specialists to combat hypertension disease. Target of Minipress is to control level of blood pressure.

Minipress acts as anti-hypertension remedy. Minipress operates by reducing blood pressure.

Minipress is also known as Prazosin, Prazopress, Vasoflex, Hypovase.

Minipress is alpha blocker.

Generic name of Minipress is Prazosin (oral).

Brand name of Minipress is Minipress.


You should take it by mouth with water.

It is better to take Minipress 2-3 times a day at the same time with meals or milk.

It is better to start the first Minipress dose when are going to bed.

If you want to achieve most effective results do not stop taking Minipress suddenly.


If you overdose Minipress and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Minipress overdosage: feeling lightheaded, rash, weakness, troublesome breathing, pruritus, swelling.


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children in a container that small children cannot open.

Side effects

The most common side effects associated with Minipress are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.


Do not take Minipress if you are allergic to Minipress components.

Be careful with Minipress if you're pregnant or you plan to have a baby, or you are a nursing mother.

Be careful with Minipress if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Minipress if you have allergies to medicines, foods, or other substances.

Be careful with Minipress if you have liver or kidney disease, heart failure, low blood pressure, narcolepsy, prostate cancer.

Be careful with Minipress if you take muscle relaxants as carisoprodol; anti-anxiety drugs as diazepam; anti-seizure drugs as carbamazepine; tranquilizers; sleep medicines as sedatives; antihistamines as diphenhydramine; verapamil; psychiatric medicines as tricyclic antidepressants (amitriptyline), phenothiazines (chlorpromazine); sexual function problems drugs as vardenafil, sildenafil, tadalafil; narcotic pain relievers as codeine; beta blockers as metoprolol, propranolol, atenolol.

Avoid machine driving.

Use Minipress with great care in case you want to undergo an operation (dental or any other).

Avoid alcohol.

Minipress can be not safety for elderly people.

Try to be careful with sunbeams. Minipress makes skin sensitive to sunlight. Protect skin from the sun.

Do not stop taking Minipress suddenly.

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Doxazosin XL may be an effective alternative to prazosin for the treatment of some PTSD symptoms.

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Employing a two-lever, food-reinforced FR10 procedure, rats were trained to recognize a discriminative stimulus (DS) elicited by the 5-HT(2A) receptor antagonist and potential antipsychotic agent, MDL100,907 (0.16 mg/kg, i.p.). In generalization tests, by analogy to MDL100,907 itself (Effective Dose(50) (ED(50)), 0.002 mg/kg, s.c.), the 'atypical' antipsychotic, clozapine, which displays high affinity for 5-HT(2A) as compared to D(2) receptors, dose-dependently and fully generalized to MDL100,907 (ED(50), 0.2 mg/kg, s.c.). S16924 (0.05 mg/kg, s.c.), S18327 (0.09 mg/kg, s.c.), quetiapine (1.8 mg/kg, s.c.), risperidone (0.02 mg/kg, s.c.) and ziprasidone (0.01 mg/kg, s.c.), antipsychotics which possess-like clozapine-marked affinity for 5-HT(2A) versus D(2) receptors, also generalized to MDL100,907. In distinction, raclopride, an antipsychotic which selectively interacts with D(2) versus 5-HT(2A) receptors, did not display significant generalization. Interestingly, haloperidol, which shows only modest affinity for 5-HT(2A) versus D(2) sites, generalized to MDL100,907 (ED(50), 0.02 mg/kg, s.c.). In light of the antagonist properties of haloperidol, clozapine and all other antipsychotics tested (except raclopride) at alpha(1)-adrenoceptors (ARs), the selective alpha(1)-AR antagonists, prazosin and WB4101, were examined. Both dose-dependently and fully generalized to MDL100,907 (ED(50)s, 0.07 and 0.11 mg/kg, s.c., respectively). At doses showing pronounced generalization to MDL100,907, the only drugs which significantly suppressed response rates were haloperidol and, weakly, quetiapine. Raclopride also markedly decreased response rates. In conclusion, the antipsychotic agents, clozapine, ziprasidone, risperidone, S16924, S18327, quetiapine and haloperidol, all generalized to a DS elicited by MDL100,907. While D(2) receptors are not implicated in their actions, in addition to antagonist properties at 5-HT(2A) receptors, blockade of alpha(1)-ARs and other, as yet unidentified, mechanisms may be involved. These data underpin interest in MDL100,907 as a potential antipsychotic agent.

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Adrenergic receptor binding characteristics were analyzed in the mutant mouse tottering (tg/tg), a single gene locus autosomal recessive mutation causing hyperinnervation by locus coeruleus neurons of their target regions, which results in epilepsy. Instead of the expected down-regulation of receptors due to the hyperinnervation, both [3H]prazosin (alpha 1-receptor) and [125I]iodopindolol (beta-receptor) binding were normal in the tg/tg hippocampus, spinal cord and slightly increased in the cerebellum. This lack of postsynaptic receptor modulation in the target cells, combined with increased levels of norepinephrine due to the aberrant axon growth, may the critical factors in the expression of the abnormal spike-wave absence seizures in the tg/tg mouse.

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The effects of peptidoleukotrienes (LTs) on electrically driven guinea pig left atria (GPLA) were investigated. LTD4 produced a positive inotropic response; however, rapid desensitization required the construction of noncumulative dose-response curves to naive tissues. The maximal inotropic response to LTD4 was 24 +/- 3% of isoproterenol and the EC50 = 267 +/- 77 nM. The functional response was corroborated by the demonstration of specific and rapid [3H]LTD4 binding to GPLA membranes with low affinity (Kd = 212 +/- 80.2 nM), in a saturable (Bmax = 20 +/- 1.1 pmol/mg protein) manner. In tissues pretreated with acivicin, which inhibits conversion of LTC4 to LTD4, the response to LTC4, but not LTD4, was abolished. Selectivity towards LTD4 was demonstrated by the inability of propranolol, prazosin, atropine, pyrilamine, capsaicin or indomethacin (all tested at 1 microM) to alter the functional response to LTD4. Similarly, none of the tested compounds (100 microMs) was inhibitory in the binding assay. Structurally diverse LTD4 antagonists SKF102922 (pKb = 6.42) and ICI 198.615 (pKb = 8.74) were able to inhibit the functional response as well as [3H]LTD4 binding to GPLA membranes. The calcium channel antagonist, verapamil, inhibited the functional response but did not alter [3H]LTD4 binding. These data support the existence of specific LTD4 receptors in GPLA which evoke a modest, rapidly desensitized, increase in the force of myocardial contraction.

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The effects of alpha-adrenoceptors agents on seizures induced by intraperitoneal administration of lidocaine (75 mg/kg) were studied in mice. Pretreatment with the selective alpha 2-adrenoceptor agonist, tizanidine, decreased the incidence of seizures induced by lidocaine. Tizanidine increased the latency to the first seizure in those animals which progressed to seizures. The blockade of alpha 2-adrenoceptors with yohimbine or phentolamine counteracted the protection induced by tizanidine. The selective alpha 2-adrenoceptor antagonist, prazosin, did not modify the protection induced by tizanidine. The alpha 2-adrenoceptor agonist clonidine also increased the latency to the first seizure induced by lidocaine. The protective effect of clonidine was also reversed by pretreatment with the selective alpha 2-adrenoceptor antagonist yohimbine. Taken together, these results suggest that alpha 2-adrenoceptors are involved in seizures induced by lidocaine.

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The present study was aimed at investigating in rats whether a common mechanism might underlie the reversal of depressive-like behaviors by classical antidepressants and by GABA agonists such as muscimol. Blockade of GABA transmission with picrotoxin (1 mg/kg IP) abolished the muscimol (0.5-1 mg/kg)-induced reduction of immobility in the swimming test and the reversal of escape failures in the learned helplessness paradigm. Conversely, picrotoxin was found not to reduce the efficacy of imipramine-like drugs in these same animal models. The combination of muscimol and tricyclics given at subeffective doses resulted in behavioral changes that can be accounted for by an additive interaction between these two classes of drugs. These data confirm the antidepressant-like profile of GABA agonists but suggest that it is unlikely that the primary antidepressant mechanism of conventional antidepressants involves GABA-A receptors. In the swimming test, prazosin (2 mg/kg), an alpha adrenoceptor blocker, antagonized the reduction of immobility produced by both muscimol and imipramine-like drugs. In the learned helplessness paradigm, penbutolol (0.25-0.5 mg/kg) and, though to a lesser extent prazosin, counter-acted the reversal of escape failures caused by muscimol and imipramine. On the basis of these data, it is tempting to speculate that increased transmitter outflow at noradrenergic receptors may be an essential component in the mechanism of action of imipramine-like drugs but also of GABA agonists.

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This randomized, open-label, 2-sequence, 2-period crossover study was conducted at the Urological Clinic, National Cheng Kung University Medical Center, Taman, Taiwan. Men newly diagnosed with symptomatic BPH who had not previously received treatment for BPH were recruited between August 2002 and April 2006. Patients were randomly assigned to 1 of 2 treatment sequences. Group A received generic terazosin during period 1 (6 weeks) and branded terazosin in period 2 (6 weeks); group B received the branded drug during period 1 and the generic during period 2. The 2 study periods were separated by a 1-week washout period. All treatments were given by mouth once daily (bedtime) at an initial dosage of 2 mg/d for the first 2 weeks. At the week-2 study visit in each treatment period, the dosage could be increased to 4 mg/d or decreased to 1 mg/d based on each patient's response and experience of adverse effects (AEs), based on the opinion of the investigator. Efficacy variables included the total score on the International Prostate Symptom Scale (IPSS), a 7-item instrument used to assess objective lower urinary tract symptoms, including quality of life. IPSS was measured at baseline and weeks 2 and 6 of each treatment period, and maximal and mean uroflow rates, measured at baseline and week 6. Tolerability was assessed at each time point using physical examination, including vital signs; laboratory analysis; and spontaneous reporting.

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Knowledge about the noradrenergic system in birds is very scarce even though their biological diversity and complex social behavior make them an excellent model for studying neuronal functions and developmental biology. While the role of norepinephrine has been described in depth in a large number of central and peripheral functions in mammals, reports for avian species are limited. The radioligand [(3)H]RX 821002 ([(3)H]1,4-[6,7(n)3H]-benzodioxan-2-methoxy-2-yl)-2-imidazol) has been used to map and characterize alpha(2)-adrenoceptors through the chicken brain using in vitro autoradiography and membrane homogenates binding assays. [(3)H]RX 821002 showed a saturable and high affinity binding to a site compatible with alpha(2)-adrenoceptor, and to a serotonergic component. The autoradiographic assays displayed a similar alpha(2)-adrenoceptor distribution than those previously reported in birds using other radioligands such as [(3)H]UK 14304 ([(3)H]5-bromo-N-(4,5-dihydro-1H-imidazol-2-yl)-6-quinoxalinamine) or [(3)H]clonidine. [(3)H]RX 821002 binding pharmacological characterization was carried out in different chicken brain regions using membrane homogenates for competition assays with different alpha(2)-adrenoceptor agonists and antagonists drugs (oxymetazoline, BRL 44408 [2-(2H-(1-methyl-1,3-dihydroisoindole)methyl)-4,5-dihydroimidazole] ARC 239 [2-(2-4-(O-methoxyphenyl)-piperazin-1-yl)-ethyl-4,4-dimethyl-1,3-(2H,4H)-isoquinolindione], prazosin, UK 14304 and RX 821002). The results showed alpha(2A) as the predominant alpha(2)-adrenoceptor subtype in the chicken brain while alpha(2B)- and/or alpha(2C)-adrenoceptor subtypes were detected only in the telencephalon. RX 821002, serotonin (5-HT) and 8-OH-DPAT [8-hydroxy-2-(di-n-propylamino)tetralin] competition assays, and competition binding assays performed in the presence of serotonin demonstrated that [(3)H]RX 821002 binds with higher affinity to a serotonergic component, probably 5-HT(1A) receptors, than to the alpha(2)-adrenoceptors. Similar pharmacological properties for the alpha(2)-adrenoceptor component were observed both in rat and chicken brain. The results demonstrate that the different alpha(2)-adrenoceptor subtypes are present in chicken brain and suggest that these receptors are highly conserved through evolution.

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Treatment of neuropsychiatric symptoms (NPS) represents a major clinical challenge in Alzheimer's disease (AD). Agitation and aggression are frequently seen during institutionalization and increase patient morbidity and mortality and caregiver burden. Off-label use of atypical antipsychotics for treating agitation in AD showed only modest clinical benefits, with high side-effect burden and risk of mortality. Non-pharmacological treatment approaches have become the preferred first-line option. When such treatment fails, pharmacological options are often used. Therefore, there is an urgent need to identify effective and safe pharmacological treatments for efficiently treating agitation and aggression in AD and dementia.

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Hyponatremia is a serious complication of 3,4-methylenedioxymethamphetamine (MDMA) use. We investigated potential mechanisms in two double-blind, placebo-controlled studies. In Study 1, healthy drug-experienced volunteers received MDMA or placebo alone and in combination with the alpha-1 adrenergic inverse agonist prazosin, used as a positive control to release antidiuretic hormone (ADH). In Study 2, volunteers received MDMA or placebo followed by standardized water intake. MDMA lowered serum sodium but did not increase ADH or copeptin, although the control prazosin did increase ADH. Water loading reduced serum sodium more after MDMA than after placebo. There was a trend for women to have lower baseline serum sodium than men, but there were no significant interactions with drug condition. Combining studies, MDMA potentiated the ability of water to lower serum sodium. Thus, hyponatremia appears to be a significant risk when hypotonic fluids are consumed during MDMA use. Clinical trials and events where MDMA use is common should anticipate and mitigate this risk.

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We analyzed a retrospective cohort from an administrative claims database from January 2004 through December 2010.

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We hypothesized that pacing-induced congestive heart failure alters alpha-adrenergic constriction in intrapulmonary bronchial arteries. Cumulative dose responses to norepinephrine (NE), phenylephrine (PE), acetylcholine (ACh) and sodium nitroprusside (SNP) were determined in pressurized vessel segments. ED(50) values for NE and PE were higher for control (-5.34 +/- 0.09 and -4.27 +/- 0.08 M, respectively) vs. paced (-5.73 +/- 0.10 and -5.06 +/- 0.28 M, respectively) groups. Prazosin increased the ED(50) values for NE and PE in both control and paced groups. Yohimbine decreased NE ED(50) in the control group only. Endothelium removal or nitric oxide synthase (NOS) inhibition decreased control but not paced NE ED(50). Maximum vasodilation and sensitivity (i.e., -ED(50) values) were decreased for ACh but were similar for SNP in paced vs. control groups. Secondary segments were more reactive than paired primary segments in both groups, although pacing effects on ED(50) were unrelated to branching order. In conclusion, adrenergic constriction of canine intrapulmonary bronchial arteries is predominantly mediated via alpha(1)-adrenoreceptors and is enhanced after pacing. Endothelium-derived relaxing factor(s) normally opposes alpha-adrenergic vasoconstriction but not after pacing in this vasculature.

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We studied the effects of adrenoceptor antagonists and imidazoline derivatives on endogenous adrenaline-induced inhibition of insulin release in anesthetized rats. The intracerebroventricular injection of neostigmine increased plasma levels of catecholamines and glucose but not insulin. Pretreatment with an i.p. injection with phentolamine caused a dose-dependent increase in insulin secretion. When atropine was coadministered with phentolamine, the phentolamine-induced increase in insulin secretion was inhibited. Neither phentolamine nor atropine affected plasma levels of catecholamine. Yohimbine and idazoxan, which are alpha 2-adrenoceptor antagonists, and tolazoline, a non-selective alpha-adrenoceptor antagonist, also reversed adrenaline-induced inhibition of insulin secretion. Phenoxybenzamine, prazosin, propranolol, and antazoline, an imidazoline without alpha 2-adrenoceptor activity, did not affect insulin levels. When agents were preinjected i.p. in rats that were given saline into the third cerebral ventricle, phentolamine and antazoline, but not yohimbine and idazoxan, increased plasma levels of insulin. The results suggest that the inhibition of insulin release induced by adrenaline was reversed by antagonism of alpha 2-adrenoceptors. Phentolamine and antazoline, both of which are imidazoline derivatives, induced insulin secretion independently of the adrenoceptors only under the resting conditions.

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In the present study we have characterized the hypothermic effect of the psychoactive cannabinoid HU-210, by investigating its interaction with the endogenous pyrogens, IL-1 and PGE2. We also studied the involvement of the adrenergic system in mediation of this hypothermic effect. Injection of HU-210 directly into the preoptic area caused a dose dependent reduction of rectal temperature from 37 to 32.1 degrees C. Injection of the non-psychoactive analog, HU-211 which does not bind to brain cannabinoid receptor, did not affect body temperature. Injection of the adrenergic agonists, CGP-12177 and clonidine (beta, and alpha adrenergic agonists, respectively) abrogated the hypothermia induced by HU-210. Injection of the adrenergic antagonists, prazosin (alpha 1) and propranolol (beta) enhanced the hypothermic effect of HU-210. Intracerebral administration of IL-1 or PGE2 to rats pretreated with HU-210 caused a transient inhibition of the hypothermia. The ex vivo rate of basal or bacterial endotoxin-induced synthesis of PGE2 by different brain regions, including the preoptic area was not affected by HU-210 administration. These results suggest that the synthetic cannabinoid HU-210 acts in the preoptic area, probably via the brain cannabinoid receptor to induce hypothermia. The hypothermic effect can be antagonized by adrenergic agonists and enhanced by adrenergic antagonists. HU-210 does not interfere with the pyrogenic effect of IL-1 or PGE2.

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Recently published studies have suggested that behavioral and neurochemical changes induced by selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitors are potentiated by coadministration of a 5-HT1A receptor antagonist. The potentiating effect is hypothesized to be due to antagonism of somatodendritic 5-HT1A autoreceptors. In the present study the effects of concomitant administration of a selective 5-HT reuptake inhibitor with a 5-HT1A receptor antagonist (N-[2-[4-(2-methoxyphenyl)-1-piperazinyl] ethyl]-N-(2-pyridinyl) cyclo-hexanecarboxamide (WAY 100635) or a beta-adrenoceptor and 5-HT1A/1B receptor antagonist (pindolol or (-)-penbutolol) were studied in isolated aggressive mice. WAY 100635 was inactive, but high doses of WAY 100635 produced a marked anti-aggressive effect when combined with a non-effective dose of citalopram or paroxetine. Low doses of pindolol, but not (-)-penbutolol, produced a minor but significant anti-aggressive effect in combination with citalopram or paroxetine. High doses of pindolol or (-)-penbutolol inhibited aggressive behavior, an effect which was reversed by citalopram or paroxetine. The beta-adrenoceptor antagonist, metoprolol, but not the alpha1-adrenoceptor antagonist, prazosin, facilitated the anti aggressive effect of citalopram. The significance of these findings is discussed relative to the above hypothesis.

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In this work we studied the possible interaction between cholinergic (muscarinic and nicotinic) and adrenergic (alpha 1- and beta-adrenergic) pathways of the hypothalamic ventromedial nucleus on the regulation of arterial pressure and heart rate in conscious normotensive rats. Mean arterial pressure and heart rate were recorded in rats with cerebral chronic stainless steel cannulae implanted directly into the ventromedial nucleus. The changes in arterial pressure and heart rate produced by the injection of the cholinergic agonist (carbachol or nicotine) into the ventromedial nucleus were studied before and after the injection of prazosin (an alpha 1-adrenergic antagonist) or propranolol (a beta-adrenergic antagonist) into this same area. The injection of carbachol (2 nmol) or nicotine (40 mmol) into the ventromedial nucleus induced pressor and tachycardia responses. Previous treatment with prazosin or propranolol blocked the pressor response to carbachol and nicotine. Propranolol also abolished the tachycardic response to carbachol or nicotine, but prazosin reduced only the tachycardia produced by carbachol into the ventromedial nucleus. These results show an interaction between cholinergic and adrenergic pathways of the ventromedial nucleus affecting cardiovascular regulation and suggest that the alpha 1- and beta-adrenoceptors of this nucleus are involved in these responses.

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5-Hydroxytryptamine (5-HT) stimulates the rate and force of cardiac contraction. However, the molecular mechanisms of 5-HT actions on the heart are unknown. We examined effects of 5-HT on phospholipase C-mediated hydrolysis of phosphoinositides and its regulation in cultured fetal mouse ventricular myocytes labeled with [3H]inositol. Accumulation of inositol monophosphate, inositol bisphosphate, and inositol trisphosphate was assessed after stimulation with 5-HT, catecholamines, and AlF4-. Inositol bisphosphate and trisphosphate reached a peak at 15 minutes by 5-HT stimulation and at 30 minutes by AlF4- stimulation. Inositol monophosphate accumulated linearly for at least 30 minutes in the presence of LiCl. The 5-HT effect was dose dependent, and the threshold concentration was 0.1 microM with the half-maximum effective concentration of 1 microM. Ketanserin in nanomolar concentrations inhibited the phospholipase C reaction by 100 microM 5-HT with the half-maximum inhibitory concentration of 0.5 nM. Pertussis toxin (100-1,000 ng/ml) did not influence the phospholipase C reaction by 5-HT, but it partially inhibited the reaction by AlF4-. Protein kinase C-activating phorbol esters like 12-O-tetradecanoylphorbol 13-acetate (TPA) and phorbol 12,13-dibutyrate, but not 4 alpha-phorbol 12,13-didecanoate, which is inactive for protein kinase C, completely inhibited the reaction by 5-HT; TPA showed 30% inhibition on the reaction by AlF4-. The magnitude of accumulated inositol phosphates by AlF4- was at least several times greater than that by 5-HT. Norepinephrine- and epinephrine-stimulated phospholipase C reactions were completely abolished by prazosin. These results suggest that 5-HT directly stimulates phospholipase C-mediated hydrolysis of phosphoinositides through 5-hydroxytryptamine-2 (5-HT2) receptors in the ventricular myocytes and that this reaction is negatively regulated by protein kinase C. 5-HT2 receptors may be coupled to phospholipase C via a pertussis toxin-insensitive GTP-binding protein in the myocytes.

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Using radioligand binding techniques we studied whether alpha 1a- and alpha 1b-adrenoceptor recognition sites can be regulated independently by drugs and hormones. In rat cerebral cortex subchronic treatment with reserpine enhanced the number of [3H]-prazosin binding sites and the proportion of alpha 1b binding sites. Desipramine treatment which did not alter Bmax values, increased the proportion of alpha 1a and decreased alpha 1b binding sites. In rat myocardium hypothyroidism decreased alpha 1b-adrenoceptor binding sites. These results suggest that alpha 1-adrenoceptors are regulated in a subtype-selective manner.

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35% of patients were responsive (BP<130/85 mmHg) to add-on treatment with doxazosin (CI 90%: 30.3%-40.4%; P<0.05, stat. an. intention to treat). During the run-in phase with placebo, mean SBP/DBP (+/-SD) decreased from 155.6+/-13.2/91.8+/-6.8 mmHg (Week -3) to 151.9+/-12.9/90.1+/-7.2 mmHg (Week -1) and to 151.2+/-11.5/90.1+/-6.9 mmHg (Week 0). During add-on treatment with doxazosin, mean SBP/DBP (+/-SD) further decreased to 144.9+/-15.2/86.3+/-8.3 mmHg (Week 4), 139.7+/-15.3/83.4+/-7.9 mmHg (Week 8), 135.5+/-14.3/81.7+/-7.6 mmHg (Week 12) and 136.4+/-14.5/81.0+/-7.0 mmHg (Week 16). Overall, mean BP changes reached a plateau of about -15 mmHg (SBP) and -9 mmHg (DBP) after 16 weeks of treatment; at each visit the mean decreases from baseline were statistically significant. The following mean values of metabolic parameters were reduced during the study: fasting plasma glucose (-4.1mg/dl; -2.8%), fasting insulin (-2 microU/ml; -12.3%; P<0.05), glycated hemoglobin (-0.12%; -1.7%), HOMA-R (-1.03; -18.2%; P<0.05), total cholesterol (-1.85 mg/dl; -1.1%), LDL cholesterol (-1.35 mg/dl; -0.8%) and triglycerides (-5.64 mg/dl; -2.4%); mean HDL cholesterol increased (+1.79 mg/dl; +3.9%; P<0.01). At the end of study treatment, the percentage of patients with lab values returned within normal ranges, in comparison with basal values, was statistically significant (P<0.05) for the following parameters: fasting plasma glucose (6.3%), fasting insulin (7.5%), LDL cholesterol (6.0%). Ten-year CHD risk (+/-SD) decreased from 16.4+/-7.8% to 13.6+/-7.4% (final vs. basal: -2.87+/-3.9; -17%; P<0.01). Six patients (2.3%) reported 8 adverse drug reactions: dizziness (3), edema (2), headache (2), asthenia (1). In one out of these 6 patients, in whom doxazosin was associated to the ACE inhibitor quinapril, adverse reaction (peripheral edema) led to treatment withdrawal.

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1. The effectiveness of alpha 1- and alpha 2-adrenoceptor activation was compared at different levels of the saphenous and cephalic vein of the dog in vitro. 2. Helically cut strips were used to determine concentration-response curves to phenylephrine, noradrenaline, UK-14,304 (5-bromo-6-(imidazoline-2-ylamino)-quinoxaline) and B-HT 920 (2-amino-6-allyl-5,6,7,8-tetra-hydro-4H-(thiazo)-4,5-d-azepine). The effect of prazosin and yohimbine on these curves was also studied. 3. At the distal level, the maximum response to UK-14,304 amounted to 33 and 50% of those to noradrenaline in the saphenous and cephalic vein, respectively, while at the proximal level the maximum response to UK-14,304 amounted to 72 and 78% of those to noradrenaline, in the saphenous and cephalic vein, respectively. 4. In both vessels, the results obtained with B-HT 920 were very similar to those for UK-14,304. 5. The pD2 values for UK-14,304 - which were identical at the three levels of both vessels - and the pA2 values for the antagonism exerted by either prazosin or yohimbine against the responses to UK-14,304 indicate that the alpha 2-adrenoceptors are identical at the different levels of both vessels. 6. These results show that the effectiveness of alpha 2-adrenoceptor stimulation increases from the distal to the proximal regions of canine limb veins. Apparently, this is due to a greater density of alpha 2-adrenoceptors in the proximal regions. 7. Yohimbine is much more potent against phenylephrine distally than proximally in both vessels. However, after 30 nm phenoxybenzamine - a concentration which eliminates the vast majority of alpha,-adrenoceptors without affecting alpha 2-adrenoceptors - yohimbine became equally potent at both levels, suggesting that the difference existing before phenoxybenzamine depended on alpha,-adrenoceptors. Hence it is concluded that alpha,-adrenoceptors in distal and proximal portions may differ.

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In human kidney, we found unique prazosin-binding sites that were insensitive to phentolamine and were thus unlikely to be alpha(1)-adrenoceptors. As the binding of [(3)H]prazosin to phentolamine-insensitive sites was prevented by 100 microM guanabenz, the insensitive sites were evaluated by subtracting [(3)H]prazosin binding in the presence of 100 microM guanabenz from that in the presence of 10 microM phentolamine. [(3)H]Prazosin bound to the phentolamine-insensitive sites monophasically with a high affinity (pK(d); 9.1+/-0.08, n=8), and the B(max) value (814+/-204 fmol mg(-1) protein, n=8) was more than ten times that of the phentolamine-sensitive alpha(1)-adrenoceptor (pK(d)=9.9+/-0.13, B(max)=66+/-23 fmol mg(-1) protein, n=7). The phentolamine-insensitive sites in human kidney were highly sensitive to other quinazoline derivatives such as terazosin and doxazosin. However, other alpha(1)-adrenoceptor antagonists (tamsulosin, WB4101 and corynanthine) did not inhibit the binding at a range of concentrations that generally exhibit alpha(1)-adrenoceptor antagonism, and noradrenaline, rauwolscine and propranolol were without effect on the [(3)H]prazosin binding. On the other hand, ligands for the renal Na(+)-transporter (amiloride and triamterene) and for imidazoline recognition sites (guanabenz, guanfacine and agmatine) displaced the binding of [(3)H]prazosin to phentolamine-insensitive sites at micromolar concentrations. Photoaffinity labeling with [(125)I]iodoarylazidoprazosin showed phentolamine-insensitive labeling at around 100 kDa, a molecular size larger than that of human alpha(1a)- and alpha(1b)-adrenoceptors expressed in 293 cells (50-60 and 70-80 kDa, respectively) on electrophoresis. In contrast, there was no detectable phentolamine-insensitive binding site but were phentolamine-sensitive alpha(1)-adrenoceptors in human liver (pK(d)=10.0+/-0.06, B(max)=44+/-6 fmol mg(-1) protein, n=3). Phentolamine-insensitive prazosin binding sites were also detected in rabbit kidney (approximately 50% of specific binding sites) but were minor in rat kidney (less than 20%). In conclusion, there are unique prazosin-binding sites in human kidney, the pharmacological profiles of which were distinct from those of known adrenoceptors.

minipress drug interactions

Lower urinary tract symptoms (LUTS) suggestive of benign prostatic obstruction are common in aging men. Nearly 25% of men >40 years of age have LUTS. Medical therapy with alpha-blockade is the most common method of medical therapy for benign prostatic obstruction. Multiple methods of minimally invasive surgical therapies have been introduced in the last decade. These methods include balloon dilatation, temporary and permanent urethral stents, various laser techniques, microwave thermotherapy, transurethral needle ablation, electrovaporization, and high-intensity focused ultrasound. alpha-Receptor blockers to reduce the sympathetic tone of the prostate are considered as first-line therapy to relieve the symptoms of benign prostatic hyperplasia. Selective alpha(1)-receptor blockers relax prostatic smooth muscle, relieve bladder outlet obstruction, and enhance urine flow with fewer side effects. In addition, it was determined that treating patients with alpha-blockers increases prostatic apoptosis. Pharmacokinetic activity, mode of action, clinical efficacy, and side effects of the selective alpha(1)-receptor blockers terazosin, doxazosin, and prazosin are reviewed.

minipress medication information

The present study investigates the role of the two putative amine transmitters (norepinephrine and serotonin) in mediating the facilitatory action following locus coeruleus (LC) stimulation on hindlimb flexor and extensor monosynaptic reflexes (MSRs) in unanesthetized, decerebrate cats. When administered sequentially, in either order, methysergide (a serotonergic blocker) and prazosin (an alpha 1-adrenergic blocker) were observed to cause subtotal, decremental changes in the potentiation of gastrocnemius-soleus and common peroneal MSRs by stimuli applied in the LC. These changes were determined to be independent of the blood pressure changes induced by the aminergic blockers. These results support the hypothesis that the facilitation of the group Ia reflex transmission in cat spinal cord by stimulation of LC is mediated in part by alpha 1-noradrenergic and serotonergic mechanisms.

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1. The pharmacokinetic and pharmacodynamic profiles of intravenous and oral doxazosin were investigated in 6 normotensive volunteers. 2. The pharmacokinetics of i.v. and oral doxazosin were fitted simultaneously and independently. The parameters derived were in good agreement with a mean elimination half-life of 539 +/- 75 min, bioavailability of 0.65 +/- 0.11 and clearance of 140 +/- 26 ml/min. 3. Pharmacokinetic-pharmacodynamic modelling indicated that the sensitivities to oral and i.v. doxazosin in individual subjects were in good agreement. 4. Based on these findings it is unlikely that doxazosin metabolites contribute significantly to the pharmacodynamic profile of doxazosin.

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1. The effects of intravenous captopril and enalaprilic acid on the increase in pulmonary inflation pressure induced by different bronchoconstrictor agents were evaluated in the anaesthetized guinea-pig. 2. Captopril and enalaprilic acid (1.6-200 micrograms kg-1) enhanced dose-dependently the bronchoconstriction (BC) induced by substance P. The threshold effective dose was 1.6 micrograms kg-1 and maximal potentiation over the control response was more than 400% for both agents. Enalaprilic acid was also assayed for serum and lung angiotensin converting enzyme (ACE) inhibition in anaesthetized guinea-pigs. This drug produced a dose-dependent inhibition of ACE in both tissues, with ED50 s of 7.6 and 9.4 micrograms kg-1, respectively: this inhibitory activity was positively correlated to substance P potentiation. 3. Captopril (8-1000 micrograms kg-1) enhanced dose-dependently the BC induced by capsaicin. The threshold effective dose was 40 micrograms kg-1 and maximal potentiation about 90%. 4. Captopril (200-1000 micrograms kg-1) did not affect BC induced by bradykinin. However, this response was markedly enhanced (about 200%) by captopril 200 micrograms kg-1 in propranolol-pretreated animals. 5. Captopril and enalaprilic acid (200-1000 micrograms kg-1) slightly (20-40%) but significantly enhanced the BC induced by 5-hydroxytryptamine. However, this response was potentiated to the same extent by a dose of prazosin, which produced a degree of hypotension similar to that observed after administration of the ACE inhibitors. 6. In conclusion, ACE inhibitors potentiate the BC induced by substance P and, to a minor extent, that induced by capsaicin in the anaesthetized guinea-pig. Potentiation of substance P is well correlated with ACE inhibition in guinea-pig serum and lungs. These experimental results may offer a mechanistic interpretation of cough and bronchial hyperreactivity observed in patients receiving treatment with ACE inhibitors.

minipress overdose symptoms

[(3)H]Prazosin bound to alpha(1A)- and alpha(1B)-adrenoceptors, as well as to a cimetidine-sensitive non-alpha(1)-adrenoceptor binding site in rat kidney membranes. An experimental design is presented where the alpha(1)-adrenoceptors are selectively exposed by blocking the non-alpha(1) binding site with 60 microM cimetidine. Conversely, the non-alpha(1) binding site can be selectively exposed by blocking the alpha(1)-adrenoceptors with 600 nM metitepine. The identity of the non-alpha(1) binding site for [(3)H]prazosin in the rat kidney, herein pharmacologically characterized by 33 competing substances, is still unknown.

minipress xl dosage

Systemic administrations (0.1, 0.5, and 2 mg/kg) of alpha1-adrenoreceptor (AR) antagonist prazosin dose-dependently attenuated cold allodynia in a rat tail model of neuropathic pain, whereas alpha2-AR antagonist yohimbine exacerbated it. These results suggest that the functions of alpha1- and alpha2-AR in this model are excitatory and inhibitory, respectively, consistent with their general properties. It is also proposed that cold allodynia can be reversed by alpha1-AR antagonist and exacerbated by alpha2-AR antagonist.

minipress xl drug

This study was performed to examine whether an alpha 1-constrictor tone, which limits coronary functional hyperemia during exercise, imposes a significant limitation on global cardiac performance as determined by cardiac output (CO). Seven dogs were chronically instrumented to measure left ventricular pressure (LVP), maximum rate of rise of LVP (dP/dtmax), heart rate (HR), mean aortic pressure (AoP), circumflex blood flow velocity (CFV), and CO at rest and during submaximal exercise. Either the selective alpha 1-adrenergic antagonist prazo (0.5 mg) or the vasodilator adenosine was administered into the circumflex artery during exercise at 6.4 kilometers per hour (kph)/16% treadmill incline. Exercise caused significant increase in mean AoP, HR, LVP, dP/dtmax, CFV, stroke volume (SV), and CO, whereas systemic vascular resistance (SVR) was significantly reduced. After intracoronary alpha 1-blockade with prazosin, CFV, dP/dtmax, SV, and CO increased further (17 +/- 2, 19 +/- 3, 16 +/- 2, and 17 +/- 2%, respectively) without changing mean AoP, HR, or SVR. Comparable increases were observed when CFV was increased by a similar degree using the direct vasodilator adenosine. These results indicate that increasing coronary flow by removing a coronary alpha 1-constrictor tone with prazosin or by direct vasodilation with adenosine during submaximal exercise leads to an increase in myocardial oxygen supply and, as a result, cardiac pump performance (SV and CO).

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minipress overdose death 2015-09-18

methanol root extract of Alafia barteri (ALA) (100-400 mg/kg, p.o.) was given 1 h before administration of chemical or thermal-induced nociception andhistamine/serotonin-induced inflammation. The mechanism of the antinociceptive effect was investigated through intraperitoneal injection of prazosin (62.5 pg/kg; alpha1-adrenoceptor antagonist), yohimbine (1 mg/kg; alpha2 adrenoceptor antagonist) N(G)-nitro-L-arginine (L-NNA) (20 mg/kg; nitric-oxide-synthase inhibitor), c y p r o h e p t a d i n e (10 mg/kg; 5-HT2R antagonist), glibenclamide (10 mg/kg; ATP-sensitive K+ -channel inhibitor), buy minipress online or naloxone (5 mg/kg; opioid-receptor antagonist) before the nociceptive models.

minipress 6 mg 2015-10-03

The mechanism of the antidepressant-like activity of the selective 5-hydroxytryptamine(6) (5-HT(6) receptor antagonist N-[3,5-dichloro-2-(methoxy)phenyl]-4-(methoxy)-3-(1-piperazinyl)benzenesulfonamide (SB-399885) was studied in the forced swim test in rats. SB-399885 administered intraperitoneally at a single dose of 10 mg/kg potently shortened the immobility time in rats. That potential antidepressant-like effect of SB-399885 was not modified in animals with a lesion of the 5-HT system produced by p-chloroamphetamine (p-CA, 2 x 10 mg/kg). The anti-immobility effect of SB-399885 was blocked by the dopamine D(1)- and D(2)-like receptor antagonists SCH 23390 (0.063 mg/kg) and sulpiride (10 buy minipress online mg/kg), respectively, as well as by the alpha(2)-adrenoceptor antagonist idazoxan (4 mg/kg), but it was not changed by the alpha(1)-adrenoceptor antagonist prazosin (1 mg/kg). Neither sulpiride (10 mg/kg) or idazoxan (4 mg/kg) nor SCH-23390 (0.063 mg/kg) administered jointly with SB-399885 (10 mg/kg) noticeably changed the exploratory locomotor activity of rats evaluated by the open field test. The results described in the present paper indicate that the anti-immobility activity of SB-399885 is not connected with 5-HT innervation, and that D(1)- and D(2)-like receptors and alpha(2)-adrenoceptors are involved in this action.

minipress tab 2017-04-23

Cutaneous vasoconstriction in response to local cooling is normally greater in females than in males. Cold induces amplification of alpha2-adrenoceptor affinity for norepinephrine and increases reflex sympathetic thermoregulatory output. Benzodiazepines are drugs with very well-known binding to the central and peripheral benzodiazepine receptors. Besides these effects they decrease sympathetic output and as it was shown in the last decade they act synergistically with alpha-adrenoceptors. In the present study we tested the hypothesis that the benzodiazepine diazepam interacts with an alpha-adrenoceptor mechanism at the level of microcirculation. We measured laser-Doppler blood flux changes provoked by local cooling before and after oral application of buy minipress online a low dose of diazepam (5 mg) in 9 healthy males and in 11 healthy females with regular menstrual cycles. The results of our experiments show that in females there is a significant reduction (ANOVA, p < 0.05) in laser-Doppler flux during the first four minutes of cooling after taking of diazepam. In males, there is no significant difference in the responses to cold before and after an application of diazepam. Our results suggest that diazepam, in addition to its well-known effect on BZ receptors may also interact with alpha2C-adrenoceptors in the vessel wall during local cooling.

minipress xl dose 2016-10-18

We investigated the dose-response effects of phenylephrine and antagonistic effects of prazosin on axial movement of the rat incisor and arterial blood pressure. Phenylephrine caused a temporal extrusive tooth movement and an increase in blood pressure at all doses. With increasing phenylephrine doses, the maximum extrusive tooth movement and maximum increase in blood pressure were buy minipress online enhanced. The maximum extrusive tooth movement and increase in blood pressure induced by phenylephrine were markedly suppressed after pretreatment with prazosin. These results suggested that extrusive tooth movement is closely related to the rise in blood pressure due to stimulation of vascular alpha1-receptors.

minipress 1mg capsule 2017-06-08

The mean (range) stone size was 4.2 (2-10) mm. Ten patients were admitted directly from the ER and 121 were discharged home. Of the 121 discharged patients, 48 (40%) were prescribed MET. In all, 46 patients received tamsulosin 0.4 mg and two received doxazosin 2 mg; no patient was prescribed steroids. The mean size of passed stones was statistically significantly lower than that of stones that did not pass (P < 0.05). Patients prescribed MET had a 23% chance of needing surgery, vs 32% in those not prescribed MET (P < 0.05). Seventy-one (61%) patients were followed buy minipress online up by a urologist, 27 (23%) by a primary-care physician, and eight (7%) had no further follow-up. Ultimately, 31 (23%) patients had a metabolic evaluation and it was abnormal in 29 (95%).

minipress ptsd dosage 2017-05-03

The present results buy minipress online indicate that ropivacaine constricts and bupivacaine dilates the pial vessels of the spinal cord in a concentration-dependent fashion, and the mechanisms involved in such actions do not seem to be mediated via alpha- or beta-adrenoceptor of spinal vasculature.

minipress drug information 2015-12-18

Knowledge on murine blood pressure and heart rate control mechanisms is limited. With the use of a tethering system, mean arterial pressure (MAP) and pulse interval (PI) were continuously recorded for periods up to 3 wk in Swiss mice. The day-to-day variation of MAP and PI was stable from 5 days after surgery. Within each mouse (n = 9), MAP and PI varied by 21+/-6 mm Hg and 17+/-4 ms around their respective 24-h averages (97+/-3 mm Hg and 89+/-3 ms). Over 24-h periods, MAP and PI were bimodally distributed and buy minipress online clustered around two preferential states. Short-term variability of MAP and PI was compared between the resting (control) and active states using spectral analysis. In resting conditions, variability of MAP was mainly confined to frequencies <1 Hz, whereas variability of PI was predominantly linked to the respiration cycle (3-6 Hz). In the active state, MAP power increased in the 0.08- to 3-Hz range, whereas PI power fell in the 0.08- to 0.4-Hz range. In both conditions, coherence between MAP and PI was high at 0.4 Hz with MAP leading the PI fluctuations by 0.3-0.4 s, suggesting that reflex coupling between MAP and PI occurred at the same frequency range as in rats. Short-term variability of MAP and PI was studied after intravenous injection of autonomic blockers. Compared with the resting control state, MAP fell and PI increased after ganglionic blockade with hexamethonium. Comparable responses of MAP were obtained with the alpha-blocker prazosin, whereas the beta-blocker metoprolol increased PI similarly. Muscarinic blockade with atropine did not significantly alter steady-state levels of MAP and PI. Both hexamethonium and prazosin decreased MAP variability in the 0.08- to 1-Hz range. In contrast, after hexamethonium and metoprolol, PI variability increased in the 0.4- to 3-Hz range. Atropine had no effect on MAP fluctuations but decreased those of PI in the 0.08- to 1-Hz range. These data indicate that, in mice, blood pressure and its variability are predominantly under sympathetic control, whereas both vagal and sympathetic nerves control PI variability. Blockade of endogenous nitric oxide formation by N(G)-nitro-L-arginine methyl ester increased MAP variability specifically in the 0.08- to 0.4-Hz range, suggesting a role of nitric oxide in buffering blood pressure fluctuations.

minipress reviews 2017-05-10

A prospective clinical and uroflowmetric study was conducted on 65 males with BPH treated with doxazosin 4 mg daily for 6 months. Patient mean age was 66.7 years (range buy minipress online 45-79). Clinical evaluation (IPSS and andrologic data) and blood analyses were performed before and after treatment. IPSS data were obtained according to the WHO validation and Spanish translation.

minipress overdose 2017-04-06

The alpha(1)-adrenergic mediated contraction, Ca(2+) signaling and the subcellular receptor distribution were evaluated using the Fluo-4, BODIPY-FL buy minipress online prazosin and subtype-specific antibodies.

minipress user reviews 2017-06-26

These results show that by combining selectivity for the alpha1A/1L-AR subtype with a reduction in intrinsic agonist efficacy, Ro 115-1240 has reduced haemodynamic effects while retaining to some degree the contractile effects on urethral smooth muscle. buy minipress online These studies indicate that Ro 115-1240 may be useful as a novel treatment for SUI.

tab minipress dosage 2016-01-06

Incontinence generally results from a problem either with the urethra or with the bladder. The urethra can permit urine to leak when it moves incessantly due to poor support or when it closes poorly, as can occur with a neurologic disorder. In the bladder, hyperactivity due to involuntary contractions, or low compliance, can lead to urinary incontinence. A thorough history and physical examination guide management. The history should buy minipress online elicit information that can allow the clinician to assess how severe the problem is (eg, number of pads used per day, frequency of leakage) and factors that may cause or influence the problem, such as medications used, previous surgical and obstetric history, and urologic history including prior therapy for incontinence. Information about when leakage is at its worst is useful. Leakage that worsens in winter is typically associated with detrusor instability. Leakage that worsens at night can indicate a problem with bladder compliance. Incontinence that started after the onset of an antihypertensive or antipsychotic medication may be due to alpha-receptor antagonist effects of drugs such as prazosin or chlorpromazine. Difficulty emptying the bladder may be associated with medications that block cholinergic and calcium-channel activity, such as sedatives, antidepressants, antispasmodics, antiemetics, antipsychotics, antiarrhythmics, and anticonvulsants. Mild incontinence can be managed conservatively in a primary care setting, with pelvic-floor exercise, behavior therapy, or anticholinergic therapy. Patients with severe incontinence or an unclear etiology of incontinence should be referred to a specialist for urodynamic testing.

minipress 4 mg 2015-04-16

Dexmedetomidine induced a concentration-related increase in the expression of pERK1 and 2 in rat hippocampal slices (EC50 [95% confidence interval] for pERK1, 0.97 [0.68-1.37] microm; for pERK2, 1.15 [0.62-2.14] microm). This effect was insensitive to the inhibitors of the alpha2AR-mediated signaling pathway, to prazosin, and to PP2, an inhibitor of the focal adhesion kinase-Src kinases. In contrast, it was still present in mice deleted buy minipress online for each of the alpha2AR subtypes and was markedly decreased by the antagonist of the I1-imidazoline receptors efaroxan, by phospholipase C and protein kinase C inhibitors, and by PD 098059, a direct inhibitor of ERK1 and 2 phosphorylation.

minipress xl tablets 2017-09-24

131-MIBG and octreotide have high sensitivity and accuracy in diagosing extra-adrenal paraganglioma. Surgical treatment should be buy minipress online carried out on the basis of correct drug preparation of α-receptor blocker, such as prazosin and phenoxybenzamine. Complete surgical excision is the treatment of choice for extra-adrenal paragangliomas as well as recurrent or metastatic disease, which could be resected laparoscopically. Intimate lifelong follow-up is necessary and important.

minipress dosage forms 2017-04-04

The alpha 1-adrenoceptor blocking effects of SGB-1534 on the urethral smooth muscle were compared in in vivo lower urinary tract preparations of anesthetized dogs, with the effects of other alpha 1-adrenoceptor antagonists, prazosin and bunazosin. Hypogastric nerve stimulation and selective administration of phenylephrine to the urethra and bladder through the cannulated right external iliac artery (i.a.) elicited reproducible frequency- and dose-dependent increases in intra-urethral pressure. Intra-bladder pressure was increased by the nerve buy minipress online stimulation but not by i.a. phenylephrine. SGB-1534, prazosin or bunazosin (0.1-10 micrograms/kg i.v.) dose dependently suppressed the urethral contraction evoked by the nerve stimulation and i.a. phenylephrine but did not influence the bladder contraction elicited by nerve stimulation. The alpha 1-adrenoceptor blocking potency of SGB-1534 was approximately 2.3 and 8.1 times greater than that of prazosin and bunazosin, respectively. The results indicate that alpha 1-adrenoceptors may mediate mainly the urethral contraction induced by hypogastric nerve stimulation and i.a. phenylephrine, and that SGB-1534 was more potent alpha 1-adrenoceptor blocking activity than prazosin and bunazosin in the canine urethra.

minipress overdose symptoms 2015-02-26

This study was conducted to determine the mechanism of arachidonic acid (AA) release elicited by phenylephrine (PHE) stimulation of alpha adrenergic receptor (AR), and its modulation by cyclic adenosine 3',5'-monophosphate (cAMP) in Rat-1 fibroblasts (R-1Fs) transfected with the alpha-1A, alpha-1B or alpha-1D AR. PHE increased AA release and also caused a marked accumulation of cAMP in R-1Fs expressing the alpha-1 AR subtypes, but not in those transfected with vector alone. PHE also enhanced phospholipase D (PLD), but not phospholipase A2 (PLA2) activity. The increase in PHE-induced AA release, PLD activity and cAMP accumulation differed among the various alpha AR subtypes with: alpha-1A > alpha-1B > alpha-1D AR. The effect of PHE to increase AA release was attenuated by C2-ceramide, an inhibitor of PLD; propranolol, a phosphatidate phosphohydrolase inhibitor; and RHC-80267, a diacylglycerol lipase inhibitor in R-1Fs expressing the alpha-1A AR. Forskolin, which activates adenylyl cyclase, increased cAMP accumulation and inhibited PHE-induced AA Norvasc Dosing Information release and PLD activity in alpha-1A-AR-expressing R-1Fs. 8-(4-chlorophenyl-thio)-cAMP, a nonhydrolyzable analog of cAMP, also attenuated the rise in AA release and PLD activity elicited by PHE in these cells. In contrast, SQ 22536, an adenylyl cyclase inhibitor, and KT 5720, a protein kinase A inhibitor, increased PHE-induced AA release and PLD activity in R-1Fs expressing the alpha-1A AR. These data suggest that the alpha-1A, alpha-1B and alpha-1D ARs are coupled to PLD activation and cAMP accumulation. Moreover, PHE promotes AA release in R-1Fs expressing the alpha-1A AR through PLD activation. Furthermore, cAMP generated by alpha-1A AR stimulation acts as an inhibitory modulator of PLD activity and AA release via protein kinase A.

minipress and alcohol 2016-11-10

These studies examined the effects of the alpha-adrenergic agonist clonidine on spontaneous and synaptically evoked activity in the solitary tract nucleus in superfused rat brain slices. In one group of neurons which showed no spontaneous spike activity (n = 27), clonidine superfusion induced a dose-dependent increase of postsynaptic responsiveness to input from the ipsilateral solitary tract. In another group of neurons which were spontaneously active but unresponsive to tract input (n = 20), clonidine induced Hytrin Medication Terazosin a dose-dependent depression of spontaneous discharge. A third group of neurons which were both spontaneously active and responsive to tract input (n = 11) showed primarily a depression of both activities. The neuronal responses to clonidine in all 3 groups were selectively blocked by the alpha 2-adrenoceptor antagonist yohimbine but not by the alpha 1-antagonist prazosin. These results provide insight into the possible actions of endogenous adrenergic systems in the synaptic processing of afferent sensory information within the solitary tract nucleus.

minipress tablets dose 2016-12-30

Non-invasive immobilization stress causes an increase in the plasma interleukin (IL)-6 level accompanied by increased IL-6 mRNA expression and IL-6 immunoactivity in the liver [Biochem. Biophys. Res. Commun. (1997) 238, 707-711]. In the present study, using rat primary cultured hepatocytes and non-parenchymal liver cells, the effect of norepinephrine (NE) on IL-6 mRNA expression was determined. IL-6 mRNA expression in hepatocytes, but not in non-parenchymal liver cells, increased when the cells were treated with NE. The stimulatory effect of NE was inhibited by the combined use of alpha- and beta-adrenergic antagonists. IL-6 mRNA expression in hepatocytes also increased on incubation with the culture medium of non-parenchymal liver cells treated with NE. The effect of the medium was blocked by an IL-1 receptor antagonist. Moreover, exogenous IL-1beta stimulated IL- Noroxin Online 6 mRNA expression in hepatocytes. IL-1beta was present in the medium of non-parenchymal liver cells and increased with NE-treatment. These results suggest that NE released from sympathetic nerve terminals during stress can directly increase IL-6 mRNA expression in hepatocytes and indirectly through IL-1beta production from non-parenchymal liver cells.

minipress medication 2015-12-13

The Antihypertensive and Lipid-Lowering high-risk hypertensive participants, ages > or = 55 years, designed to determine whether the incidence of fatal and nonfatal coronary heart disease (CHD) and combined cardiovascular events (fatal and nonfatal CHD, revascularization surgery, angina pectoris, congestive heart failure, and stroke) differs between diuretic (chlorthalidone) treatment and three alternative antihypertensive therapies: a calcium channel blocker (amlodipine), an ACE inhibitor (lisinopril), and an alpha-adrenergic blocker (doxazosin). The planned follow-up is an average of 6 years, to be completed March 2002 Zovirax Medication Dosage .

minipress max dose 2016-10-23

Effects of neurokinin A (NKA) on sympathetic neurotransmission were studied in rat vas deferens. Although neither prazosin, an alpha 1-adrenoceptor blocker, nor alpha, beta-methylene adenosine triphosphate, a P2-purinoceptor blocker, inhibited the NKA-induced contractions in the epididymal site, high concentration of NKA-induced contractions in the prostatic site were slightly decreased by either of the two blockers. Treatment with guanethidine, which prevents the release of sympathetic transmitters from presynaptic nerve endings, also had no effect on NKA-induced contractions in either site. To investigate the effects of NKA on the adrenergic and purinergic neurotransmission in more detail, we measured transmitter release by using [3H]norepinephrine or [14C]adenosine. Neither spontaneous or nor evoked 3H efflux, indicating NE release, was affected by NKA in either site. NKA enhanced 14C efflux, indicating ATP release, evoked by electrical stimulation in the epididymal site, which may be originated from smooth muscle. In the prostatic site, contractions induced by electrical stimulation were enhanced in spite of no increase in 3H or 14C efflux. These results suggest that: 1) NKA has no effect on presynaptic nerve terminals in both Depakote Overdose Mg sites, 2) NKA potentiates the effects of neurotransmitters in the prostatic site, and 3) NKA modulates the neurotransmissions.

minipress medicine 2017-05-22

In univariate analysis, the doxazosin for HTN group had the highest rate of adverse cardiac events in comparison to the BPH and reference groups (14.1 vs. 11.3% and 8.9%, respectively, P < 0.001). After stratifying for the degree of reversibility of perfusion defect, only Zyrtec Pill individuals with a moderate-to-severe perfusion defect in the doxazosin for HTN group had a significant increase in adverse cardiac events [hazard ratio 1.50 95% confidence interval (1.14-1.98)].

minipress nightmares dosage 2017-11-04

We conclude that MNLs cause contraction of Arjuna 500 Mg rabbit isolated aortic rings by the release of 5-HT.

minipress drug interactions 2015-04-25

A new high α(1A) adrenoreceptor (α(1A)AR) expression cell membrane chromatography (CMC) method was developed for characterization of α(1A)AR binding interactions. HEK293 α(1A) cell line, which expresses stably high levels of α(1A)AR, was used to prepare the stationary phase in the CMC model. The HEK293 α(1A)/CMC-offline-HPLC system was applied to specifically recognize the ligands which interact with the α(1A)AR, and the dissociation equilibrium constants (K (D)) obtained from the model were (1.87 ± 0.13) × 10(-6) M for tamsulosin, (2.86 ± 0.20) × 10(-6) M for 5-methylurapidil, (3.01 ± 0.19) × 10(-6) M for doxazosin, (3.44 ± 0.19) × 10(-6) M for terazosin, (3.50 ± 0.21) × 10(-6) M for alfuzosin, and (7.57 ± 0.31) × 10(-6) M for phentolamine, respectively. The competitive binding study between tamsulosin and terazosin indicated that the two drugs interacted at the common binding site of α(1A)AR. However, that was not the case between tamsulosin and oxymetazoline. The Celebrex Cost results had a positive correlation with those from radioligand binding assay and indicated that the CMC method combined modified competitive binding could be a quick and efficient way for characterizing the drug-receptor interactions.

minipress 2 mg 2016-03-28

1. The modulation of noradrenaline-induced membrane currents by papaverine was studied with the nystatin whole-cell technique in freshly isolated rabbit ear artery and portal vein cells. 2. At a holding potential of -50 mV (in potassium-free conditions), papaverine inhibited the Ca(2+)-activated inward chloride current ICl(Ca) evoked by ionophoretic application of noradrenaline in rabbit portal vein cells in a concentration-dependent (10(-5)-10(-4) M) manner. 3. With potassium-containing solutions (at 0 mV) 10(-4) M-papaverine reversibly abolished the Ca(2+)-activated outward potassium current IK(Ca) induced by noradrenaline in both Kemadrin 5 Mg protal vein and ear artery cells. Occasionally, 10(-4) M-papaverine itself activated IK(Ca) before it abolished the response to noradrenaline. 4. Higher concentrations of papaverine (up to 10(-3) M) always evoked both ICl(Ca) and IK(Ca) at -50 and 0 mV respectively, before it abolished these responses to noradrenaline in both ear artery and portal vein cells. In the presence of 10(-3) M-papaverine higher doses of noradrenaline evoked the non-selective cation current in some portal vein cells. 5. In the presence of 10(-2) M-caffeine, which elicited both IK(Ca) and ICl(Ca), papaverine (10(-3) M) failed to activate either current and 10(-3) M-papaverine reduced the caffeine-induced IK(Ca) by 94%. In contrast, IK(Ca) induced by the calcium ionophore ionomycin was unaffected by papaverine. In Ca(2+)-free, 1 mM-EGTA external solutions, 10(-3) M-papaverine still induced IK(Ca) and blocked the response to noradrenaline. 6. The alpha 1-adrenoceptor antagonist prazosin (5 x 10(-8) M) completely blocked the noradrenaline-induced IK(Ca) but currents evoked by papaverine (10(-3) M) were unaffected by prazosin. 7. It was concluded that papaverine modulated noradrenaline-induced membrane currents in vascular smooth muscle cells by releasing and depleting caffeine-sensitive intracellular Ca2+ stores.