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Adalat (Nifedipine)

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Adalat is a high-quality medication which is taken in treatment of hypertension or high blood pressure, angina or chest pain. Adalat acts by relaxing blood vessels (such as veins and arteries), which makes it easier for the heart to pump and reduces its workload.

Other names for this medication:

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Also known as:  Nifedipine.


Adalat is a perfect remedy in struggle against hypertension or high blood pressure, angina or chest pain.

Adalat acts by relaxing blood vessels (such as veins and arteries), which makes it easier for the heart to pump and reduces its workload.

Adalat is also known as Nifedipine, Nicardia, Nifedical, Procardia.

Generic name of Adalat is Nifedipine.

Brand names of Adalat are Adalat CC, Procardia, Procardia XL.


Adalat should be taken orally with or without food.

It is better to take Adalat at the same time every day. Take on an empty stomach.

Avoid grapefruit juice during treatment with Adalat.

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


If you overdose Adalat and you don't feel good you should visit your doctor or health care provider immediately.


Store at room temperature between 15 and 25 degrees C (59 and 77 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Adalat 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 Adalat if you are allergic to Adalat components.

Do not take Adalat if you're pregnant or you plan to have a baby, or you are a nursing mother. Adalat can harm your baby.

Do not use Adalat in combination with salt substitutes or potassium supplements.

If you want to achieve most effective results without any side effects it is better to avoid alcohol.

Avoid grapefruit juice during treatment with Adalat.

Try to be careful using Adalat if you suffer from kidney disease, liver disease, diseases of the heart or blood vessels (sick sinus syndrome), aortic stenosis, heart failure, low blood pressure, or coronary artery disease.

Do not stop taking Adalat suddenly.

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We investigated the effect of commonly used medications on the accumulation of ascorbic acid in human intestinal Caco-2 cells. Although ascorbic acid is negatively charged at physiological pH, anionic compounds including drugs and metabolites had little effect on its accumulation. On the other hand, hydrophobic 1,4-dihydropyridine compounds (nifedipine and nicardipine), but not other structurally unrelated calcium channel blockers, were found to be potent inhibitors. They inhibited both Na+-dependent and Na+-independent (K+ substituting Na+) accumulation of ascorbic acid. The inhibition was non-competitive with a Ki of 108 microM and 9 microM for nifedipine and nicardipine, respectively. The efflux of ascorbic acid from cells was not affected. Previously, we reported a similar inhibition of ascorbic acid accumulation by estrogens. When nifedipine and estrogens were included in the buffer together, the combined inhibitory effect was less than additive implying that they may act through the same mechanism. The potential clinical significance of dihydropyridine usage on ascorbic acid status in human needs to be considered.

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Immunosuppressive agents have been recognized as a factor affecting the soft tissues of the periodontium. However, little is known about their effect on periodontitis progression. The aim of the present study was to investigate the influence of cyclosporin A (CsA) administration, associated or not with nifedipine, on the bone loss resulting from a ligature-induced periodontitis in rats. Twenty-four adult male Wistar rats were used. After anesthesia, the mandibular first molar was randomly assigned to receive the cotton ligature in the sulcular area while the contralateral tooth was left unligated. The animals were randomly assigned to one of the following treatments: Group A--saline solution; Group B--CsA (10 mg/kg); Group C--nifedipine (50 mg/kg); Group D--CsA (10 mg/kg) plus nifedipine (50 mg/kg). Forty-five days later, the animals were sacrificed and the specimens routinely processed for serial decalcified sections. Intergroup analysis did not reveal significant differences regarding the bone loss volume in the ligated teeth between the experimental treatments (0.46 +/- 0.11, 0.63 +/- 0.32, 0.53 +/- 0.14, 0.50 +/- 0.18, for groups A, B, C and D, respectively--p > 0.05). However, intragroup analysis showed a greater bone loss volume in the ligated teeth than in the unligated ones (p < 0.05). Within the limits of the present study, the conclusion was that the administration of CsA, associated or not with nifedipine, may not influence bone loss in ligature-induced periodontitis in rats.

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Rat basilar arteries of a normal group and SAH groups (1 hour, 2 days, and 1 week) were removed from the brain and cut into spiral preparations.

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Coronary heart disease and ischemic stroke are among the leading causes of morbidity and mortality in adults, and cerebrovascular disease is associated with the presence of symptomatic and asymptomatic CHD. Several studies noted an association between coronary calcification and thoracic aorta calcification by several imaging techniques, but this association has not yet been examined in stable angina pectoris patients with the use of spiral computed tomography.

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Ursolic acid (UA) in concentrations of l x 10(7) mol/L - 5 x 10(5) mol/L induced relaxation in gastric smooth muscle (SM) tissues, in a concentration-dependent manner. The relaxation did not change membrane potential and slow wave contraction patterns. A significant decrease in amplitude and frequency of spike- potentials was observed. UA-induced reactivity was removed when SM preparations were treated with nifedipine (1 x 10(6) mol/L). Ca2+-induced contractions of the depolarized SM preparations (42 mmol/L K+; Ca2+-free Krebs solution) were substantially reduced in the presence of UA. It was determined that, in certain concentrations, UA influenced L - type Ca2+ channels, and reduced the Ca2+ influx.

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Indapamide metabolism was studies in vitro using human liver microsomes pretreated with or without different concentrations of CYP-selective inhibitors and seven major antihypertensive drugs, felodipine, nifedipine, nitrendipine, telmisartan, irbesartan, valsartan and puerarin. Furthermore, the pharmacokinetics of indapamide was determined by HPLC-MS/MS to evaluate the effects of felodipine coadministered on the bioavailability of indapamide in rats in vivo.

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These results are consistent with the hypothesis that Bay K 8644, through its facilitation of increased intracellular calcium, results in the activation of the phosphatidylinsitol-signaling pathway and cytosolic calcium oscillation-like phenomena, thereby resulting in the generation of phasic myometrial contractions.

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The severe preeclampsia group had significantly lower platelet counts, higher systolic and diastolic blood pressures and elevated serum uric acid concentrations. Pre-treatment plasma leptin levels were significantly increased in the severe preeclampsia group (range 18.3-49.5) compared to the the mild preeclampsia group (range 20.7-45.4) and normal controls (range 8.6-19.2). Post-treatment plasma leptin levels in both the mild and severe preeclampsia groups (range 10.2-23.5 and 11.3-24.4, respectively) were statistically similar to those of the control group (range 9.1-20.7). Estimated foetal weight, intrauterine growth retardation and demise were statistically similar in the three study groups.

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Maximum inhibition of contraction amplitude was 93 +/- 2% and 67 +/- 14% for progesterone at 30 microM and vehicle (70% ethanol), respectively, P < 0.05. 17OHPC did not exert an inhibitory effect. Water soluble progesterone exerted a maximal inhibitory effect on amplitude of contractions of 82 +/- 10% at 100 microM, P < 0.05. The inhibitory effect of progesterone was unaffected by potassium channel blockers. There was no difference between in vivo placebo and progesterone-treated groups in either amplitude or frequency of contractions, nor was there any difference in the response to oxytocin or the tocolytic drugs.

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In Langendorff-perfused rabbit hearts, under β-adrenergic stimulation with isoproterenol (ISO; 1 µM), 8 weeks MI decreased AF threshold, indicating increased AF susceptibility. This was associated with increased atrial action potential duration (APD)-alternans at 90% repolarization, by 147%, and no significant change in the mean APD or atrial global conduction velocity (CV; n = 6-13 non-MI hearts, 5-12 MI). In atrial isolated myocytes, also under β-stimulation, L-type Ca(2+) current (I(CaL)) density and intracellular Ca(2+)-transient amplitude were decreased by MI, by 35 and 41%, respectively, and the frequency of spontaneous depolarizations (SDs) was substantially increased. MI increased atrial myocyte size and capacity, and markedly decreased transverse-tubule density. In non-MI hearts perfused with ISO, the I(CaL)-blocker nifedipine, at a concentration (0.02 µM) causing an equivalent I(CaL) reduction (35%) to that from the MI, did not affect AF susceptibility, and decreased APD.

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Calcium entering the cell via different routes, e.g.,N-methyl-D-aspartate (NMDA) receptors or voltage-dependent calcium channels (VDCCs), plays a pivotal role in hippocampal synaptic potentiation. Since corticosteroid hormones have been reported to enhance calcium influx through VDCCs, one may predict that these hormones facilitate hippocampal synaptic efficacy. Surprisingly, though, stress and corticosteroids have so far been found to reduce synaptic potentiation. Here, we addressed this apparent paradox and examined synaptic potentiation in the CA1 area of hippocampal slices from mice with low basal corticosterone levels 1--4 h after a brief in vitro administration of corticosterone. Nifedipine and APV were used to isolate NMDA receptor-mediated and VDCC-mediated long-term potentiations (LTPs), respectively. We report that corticosterone facilitates synaptic potentiation that depends on activation of VDCCs while impairing synaptic plasticity that is mediated by NMDA receptor activation. The glucocorticoid-receptor (GR) antagonist RU 38486 blocked both the effects of corticosterone. These results indicate that the net effect of corticosteroid hormones on synaptic plasticity is determined by the balance between different types of potentiation, a balance that may be region specific and depends on the experimental conditions. We speculate that these opposite effects on synaptic efficacy are involved in the bidirectional modulation of cognitive performance by corticosteroid hormones.

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Serum estrogen was increased in OVX+EST rats (60.5 +/- 18.2 pg/mL) compared to OVX (0.2 +/- 0.2 pg/mL P < 0.05 vs OVX+EST) and CTL animals (1.3 +/- 1.0 pg/mL P > 0.05 vs OVX). OVX showed significantly less myogenic tone at 75 mm Hg (13.8 +/- 3.6%, P < 0.05 vs CTL) than CTL (29.8 +/- 4.7%) that was partially restored by estrogen therapy (21.2 +/- 4.5; P > 0.05). At serotonin concentrations of 10(-7) M, 3 x 10(-7) M, and 10(-6) M, the vessels from ischemic OVX rats showed significantly greater constriction (20.9 +/- 2.1%, 35.0 +/- 3.9%, and 39.4 +/- 3.4%, respectively) compared to nonischemic CTL rats (6.3 +/- 1.1%, 11.3 +/- 1.8%, and 16.8 +/- 2.5%, respectively P < 0.05). Estrogen therapy resulted in intermediate responses (18.2 +/- 5.3%, 25.2 +/- 6.6%, and 28.2 +/- 6.5%, respectively) that were not significantly different from the other groups. In addition, ischemia resulted in significantly greater dilation in response to 0.01 microM nifedipine in vessels from OVX animals (51.1 +/- 8.0%) compared to nonischemic CTL (18.0 +/- 3.8%; P < 0.05) and estrogen therapy resulted in an intermediate response (38.0 +/- 10.6; P > 0.05). Both reactivity to nitro-L-arginine and passive distensibility were not different among groups. There were no differences in percent infarct or neurologic deficit between ischemic groups.

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Sixteen patients with normal-tension glaucoma (mean age, 55.6+/-9.8 years; male:female ratio, 3:13) underwent color Doppler imaging to measure the resistance index, and peak systolic and end-diastolic blood flow velocities of the ophthalmic artery, central retinal artery, and nasal and temporal short posterior ciliary arteries. Measurements were taken before and during CO2 supplementation sufficient to increase the end-tidal CO2 partial pressure by 10%. The color Doppler imaging measurements were repeated after 2 to 4 weeks of treatment with 2 mg oral nilvadipine, and comparisons were made between the effects of the two treatments.

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Baseline clearance was 498.7 +/- 225.0 nl/60 min/gm (mean +/- SE). PAF at 10(-8) mol/L (n = 5) increased clearance to 3753.8 +/- 572.8 nl/60 min/gm (p < 0.01). Pretreatment with verapamil (2 mg/kg; n = 5) significantly reduced the increase in permeability caused by 10(-8) mol/L PAF (1909.1 +/- 620.2 nl/60 min/gm; p < 0.05). Nifedipine (5-10(-6) mol/L; n = 5) also significantly attenuated the impact of 10(-8) mol/L PAF (2037.2 +/- 427.5 nl/60 min/gm; p < 0.05). Neither verapamil nor nifedipine affected PAF-induced vasoconstriction.

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Over a 38-month period, 301 women were allocated to receive M (90), N (114), or I (90). Gestational age at delivery (p = 0.551) or arrest of labor >48 h, >7 days were similar between the three groups (p = 0.199, 0.654). Hypotension and tachycardia were more common in N patients compared to women receiving M or I (p = 0.003, 0.009). Patients receiving I had more fetal ductal constriction or oligohydramnios compared to M or N (p = 0.001, 0.020) but, I women were tested more often. There was one case of pulmonary edema in the M group and one with plural effusion in the N group.

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Although laser Doppler flowmetry (LDF) is widely used for measuring microperfusion, it is rarely used to measure coronary microcirculation. The present in vivo study investigated the use of LDF to measure myocardial microperfusion in beating rat hearts. Ascending aortic flow and other hemodynamic parameters were simultaneously recorded. A needle probe with a holder was adhered to the epicardium of the left ventricular myocardium close to the left anterior descending coronary artery in an anaesthetized open-chest rat. Myocardial microperfusion was measured in response to bolus intravenous administration of both two representative vasodilators (captopril and nifedipine) and a vasoconstrictor (pituitrin). Myocardial microperfusion was found to be predominately diastolic, and in an opposing phase to the ascending aortic flow. Captopril (5 or 10 mg/kg) increased the initial myocardial microperfusion phase. Nifedipine at 75 microg/kg caused a sustained myocardial microperfusion elevation with a peak increase of 7.1+/-1.1%, but this was not observed using 150 microg/kg nifedipine. Both drugs caused an increase in the cardiac index. In contrast, myocardial microperfusion decreased (28.7+/-0.1% maximum decrease) in response to 1 IU/kg pituitrin. In conclusion, LDF provided a means of assessing myocardial microperfusion in beating rat hearts, and can be applied to evaluate the coronary microcirculation response to drugs.

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To evaluate the impact of extracellular and intracellular Ca2+ on contractions induced by ethanol in smooth muscle.

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Drug metabolizing activities of cytochromes P450 (P450s, or CYPs) 3A4 and 3A5 in liver microsomes from the cynomolgus monkey [Macaca fascicularis (mf)] were investigated and compared with those of human P450 3A enzymes. Low activities for dealkylation of ethoxyresorufin and pentoxyresorufin were seen in recombinant monkey mfCYP3A4 and mfCYP3A5 and in recombinant human CYP3A4 and CYP3A5 expressed in bacterial membranes. Hydroxylation activities of mfCYP3A4 and mfCYP3A5 toward coumarin, paclitaxel, diclofenac, flurbiprofen, and S-mephenytoin were below detectable levels, as was also true for CYP3A4 and CYP3A5. Monkey mfCYP3A5 and mfCYP3A4 were highly active in bufuralol 1'-hydroxylation. mfCYP3A5 was efficient at dextromethorphan O-demethylation, although human CYP3A5 was unable to catalyze this reaction. Apparent bufuralol 1'-hydroxylation and dextromethorphan O-demethylation activities of monkey liver microsomes were higher than those of human liver microsomes, possibly because of contributions of mfCYP3A5 to these P450 2D-dependent drug oxidations. mfCYP3A5 and CYP3A5 catalyzed midazolam 1'-hydroxylation at a low substrate concentration more efficiently than the corresponding CYP3A4. mfCYP3A5 had higher testosterone 6beta-hydroxylase activity than mfCYP3A4, but the reverse relationship was observed in oxidation of nifedipine and hydroxylation of dexamethasone. These results demonstrate that monkey P450 3A enzymes have similar substrate selectivity to that of human P450 3A enzymes, but exhibit wider substrate selectivity toward P450 2D substrates.

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Cytoplasmic calcium (Ca(2+)) mobilization has been proposed to be an important factor in the induction of emesis. The selective sarcoplasmic/endoplasmic reticulum Ca(2+)-ATPase (SERCA) inhibitor thapsigargin, is known to deplete intracellular Ca(2+) stores, which consequently evokes extracellular Ca(2+) entry through cell membrane-associated channels, accompanied by a prominent rise in cytosolic Ca(2+). A pro-drug form of thapsigargin is currently under clinical trial as a targeted cancer chemotherapeutic. We envisioned that the intracellular effects of thapsigargin could cause emesis and planned to investigate its mechanisms of emetic action. Indeed, thapsigargin did induce vomiting in the least shrew in a dose-dependent and bell-shaped manner, with maximal efficacy (100%) at 0.5 mg/kg (i.p.). Thapsigargin (0.5 mg/kg) also caused increases in c-Fos immunoreactivity in the brainstem emetic nuclei including the area postrema (AP), nucleus tractus solitarius (NTS) and dorsal motor nucleus of the vagus (DMNX), as well as enhancement of substance P (SP) immunoreactivity in DMNX. In addition, thapsigargin (0.5 mg/kg, i.p.) led to vomit-associated and time-dependent increases in phosphorylation of Ca(2+)/calmodulin kinase IIα (CaMKIIα) and extracellular signal-regulated protein kinase 1/2 (ERK1/2) in the brainstem. We then explored the suppressive potential of diverse chemicals against thapsigargin-evoked emesis including antagonists of: i) neurokinin-1 receptors (netupitant), ii) the type 3 serotonin receptors (palonosetron), iii) store-operated Ca(2+) entry (YM-58483), iv) L-type Ca(2+) channels (nifedipine), and v) SER Ca(2+)-release channels inositol trisphosphate (IP3Rs) (2-APB)-, and ryanodine (RyRs) (dantrolene)-receptors. In addition, the antiemetic potential of inhibitors of CaMKII (KN93) and ERK1/2 (PD98059) were investigated. All tested antagonists/blockers attenuated emetic parameters to varying degrees except palonosetron, however a combination of non-effective doses of netupitant and palonosetron exhibited additive antiemetic efficacy. A low-dose combination of nifedipine and 2-APB plus dantrolene mixture completely abolished thapsigargin-evoked vomiting, CaMKII-ERK1/2 activation and SP elevation. In addition, pretreatment with KN93 or PD98059 suppressed thapsigargin-induced increases in SP and ERK1/2 activation. Intracerebroventricular injection of netupitant suppressed vomiting caused by thapsigargin which suggests that the principal site of evoked emesis is the brainstem. In sum, this is the first study to demonstrate that thapsigargin causes vomiting via the activation of the Ca(2+)-CaMKII-ERK1/2 cascade, which is associated with an increase in the brainstem tissue content of SP, and the evoked emesis occurs through SP-induced activation of neurokinin-1 receptors.

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Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.

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The systemic use of a dihydropyridine CA in a clinical trial could reduce the incidence of early autoarterial conduit dysfunction and improve prognosis in the patients.

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The reaction of 2-nitrobenzaldehyde with methyl propiolate and ammonium acetate in acetic acid yields 2,6-dinor-nifedipine (1a) and as a by-product not the dimethyl 2,5-dicarboxylate isomer, but the rac. 1,2-dihydropyridine (DHP) 1b, as proven by X-ray analysis. The benzo[h][1,6]naphthyridines 4-6 are synthesized from the oxidation product 2b and the photo-product 3b. The compounds 6 represent starting materials for potential anti-malarial agents.

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Near the base of mammalian seminiferous epithelium, Sertoli cells are joined by tight junctions, which constitute the blood-testis barrier. Differentiating germ cells are completely enveloped by Sertoli cells and must traverse the tight junctions during spermatogenic cycle. Following the specific ligand activation of L-selectin, the up-regulated Rho family small G-proteins have been implicated as important modulators of tight junctional dynamics. Although the activation of L-selectin transmits subsequent intracellular signals in a Ca(+2)-dependent fashion in various cell types, little is understood regarding the signaling pathways utilized by L-selectin in Sertoli cells. Therefore, we have examined the possible resultant calcium influx triggered by specific ligand-activation of cell surface L-selectin receptors or by cross-linking of L-selectin with anti-L-selectin. Spectrofluorimetric studies demonstrate increase of intracellular Ca(+2) levels immediately after the treatment of the L-selectin ligands, fucoidan and sialyl Lewis-a, or after treatment with anti-L-selectin antibody. We then determined the mechanism of Ca(+2) influx by investigating L- and T-type voltage-operated Ca(+2) channels, which have been suggested to present in the membranes of Sertoli cells. Data demonstrate that Sertoli cells treated with L-type voltage-operated Ca(+2) channel antagonists, nifedipine, diltiazem, or verapamil, lead to dose-dependent blockage of L-selectin-induced Ca(+2) influx. Cells treated with mibedradil, a T-type voltage-operated Ca(+2) channel antagonist, results in little or no blocking effect. Therefore, we conclude that activation of Sertoli cell L-selectin induces Ca(+2) influx, which is at least partially regulated by L-type voltage-operated Ca(+2) channels.

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Many anticonvulsants are used in disorders other than epilepsy. For example, lamotrigine is reported to be effective in post-traumatic stress disorder and mania.

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adalat xl reviews 2015-07-19

1. Whole-cell Ca2+ currents (ICa) from cultured rat melanotrophs were identified by their sensitivity to Ca2+ channel blockers, and their modulation by serotonin (5-HT) was studied. All cells displayed high voltage-activated (HVA; > -30 mV) Ca2+ currents. A low voltage-activated (LVA; > -60 mV) Ca2+ current was detected in 92% of the cells. 2. The whole-cell ICa was insensitive to omega-conotoxin GVIA (0.5-1 microM) indicating the absence of N-type Ca2+ channels. 3. At a holding potential (Vh) of -70 mV, the L-type channel blocker nifedipine reduced ICa in a dose-dependent manner with a half-maximal effective concentration (IC50) of 28 nM. The L-type current represented 39% of the total ICa. 4. omega-Agatoxin IVA (omega-Aga IVA) produced a biphasic dose-dependent inhibition of ICa, with IC50 values of 0.4 and 91 nM, indicating the presence of P-type and Q-type Ca2+ channels, which accounted respectively for 16 and 45% of the total ICa. The P-type current was also blocked by synthetic funnel-web spider toxin (sFTX 3.3; 1-10 microM) and was present only in a subpopulation (60-70%) of cells. 5. All cells possessed a Ca2+ current which was resistant to nifedipine (10 microM) and omega-Aga IVA (50 nM). This current was not affected by Ni2+ (40 microM) but was abolished by a low concentration of Cd2+ (10 microM) and by omega-conotoxin MVIIC (1 microM) indicating that it was a Q-type Ca2+ current. 6. 5-HT (10 microM) inhibited the whole-cell ICa in 70% of the cells tested ( buy adalat online n = 120) by activating 5-HT1A and 5-HT2C receptors. 5-HT produced either a kinetic slowing of the activation phase (37% of the cells) or a scaling down (14% of the cells) of ICa. In the majority of cells (49%) both types of inhibition were found to coexist. 7. The effects of 5-HT were voltage dependent, rendered irreversible when GTP-gamma-S (30 microM) was present in the pipette solution and abolished by pretreatment of the cells with pertussis toxin (PTX; 150 ng ml-1, 18 h). 8. Low concentrations of omega-Aga IVA (20 nM), which blocked mainly P-type channels, did not reduce the effect of 5-HT on ICa. The scaling down effect of 5-HT on ICa was eliminated in the presence of nifedipine (10 microM) and the kinetic slowing effect of 5-HT persisted after blockade of L- and P-type channels but was abolished by omega-conotoxin MVIIC (1 microM). 9. We conclude that rat melanotrophs possess functional L-, P- and Q-type Ca2+ channels and that 5-HT inhibits selectively L-type and Q-type Ca2+ currents with different modalities. These effects are voltage dependent and mediated by a PTX-sensitive G-protein.

adalat 60 mg 2016-12-20

The oxygen deficiency seen in solid tumors is predominantly caused by an insufficient O2 supply as a result of inadequate tumor perfusion. The aim of this study was to analyze whether a number of vasodilator drugs might be suitable to increase tumor perfusion and consequently improve the oxygenation status of experimental tumors. Rats with s.c. DS-sarcomas were treated with either Na+-nitroprusside (7-25 microg x min(-1) x kg(-1) BW) or nifedipine (10 microg x min(-1) x kg(-1) BW). Red blood cell (RBC) flux was assessed continuously using laser-Doppler flowmetry and mean tumor pO2 was measured polarographically using O2-sensitive catheter electrodes. Systemic application of the vasodilator drugs resulted in a dose-dependent decrease in MABP. In parallel, tumor perfusion was reduced linearly with falling MABP resulting in a decrease in RBC flux by approximately 40%. Resistance to flow did not change during the infusion indicating that these drugs have no impact on tumor vessel diameter. With decreasing tumor perfusion, tumor pO2 was reduced parallel to the MABP drop. This effect was more distinct with Na+-nitroprusside than with nifedipine due to the more pronounced fall in MABP. The vasodilator drugs studied are buy adalat online not suitable for dilation of tumor vessels either because the tumor vasculature lacks contractile wall elements or because the vessels are already maximally dilated.

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A. membranaceus increases the atrial dynamics via Na+ -Ca2+ exchanger and L-type Ca2+ channel buy adalat online and negatively modulates ANP secretion in beating rabbit atria.

adalat tab 2015-01-02

The immunosuppressive interactions of calcium channel antagonists [diltiazem (Dil), verapamil (Ver) and nifedipine (Nif)], with corticosteroids [methylprednisolone (Mpl), prednisolone (Prd)], and macrolides [tacrolimus (Tac buy adalat online ) and sirolimus (Sir)] were examined in human whole blood lymphocyte cultures. Gender-related differences in responses in the interactions between these drug classes were studied using blood from 6 males and 6 females. The nature and intensity of interactions were determined using an extended Loewe additivity model. All immunosuppressants exhibited higher potency than the calcium channel antagonists with mean IC50 values of: Dil Ver Nif Mpl Prd Tac Sir (mM) (mM) (mM) (nM) (nM) (nM) (nM) Male 135 41.9 213 12.1 18.6 150 327 Female 114 31.8 47.4 4.6 8.8 111 106 Gender-related differences in responses to Mpl and Prd were observed while the others were not significant. Additive interactions were found among calcium channel antagonists and corticosteroids. Significant synergistic interactions were observed between calcium channel antagonists and tacrolimus and sirolimus, although these are unlikely to be of clinical importance. These studies demonstrate diverse drug interactions in the examination of an important array of immunosuppressant drug combinations.

adalat tablets 2015-07-19

The tissue was obtained from 12 patients with chronic erectile dysfunction. The buy adalat online effects of Ca2+-free solution, ryanodine, caffeine and of nifedipine on electrically and adrenergically induced contractions were evaluated.

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I was recorded from acutely isolated rat dorsal root ganglion neurons using the whole cell patch clamp technique before, during, and after application buy adalat online of the micro -opioid agonist fentanyl (0.01-1 micro m). Capsaicin was applied to each cell at the end of the experiment.

adalat 40 mg 2015-11-26

Previous work from this laboratory demonstrated that arachidonic acid activates c-jun NH(2)-terminal kinase (JNK) through oxidative intermediates in a Ca(2+)-independent manner (Cui X and Douglas JG. Arachidonic acid activates c-jun N-terminal kinase through NADPH oxidase in buy adalat online rabbit proximal tubular epithelial cells. Proc Natl Acad Sci USA 94: 3771-3776, 1997.). We now report that JNK can also be activated via a Ca(2+)-dependent mechanism by agents that increase the cytosolic Ca(2+) concentration (Ca(2+) ionophore A(23187), Ca(2+)-ATPase inhibitor thapsigargin) or deplete intracellular Ca(2+) stores [intracellular Ca(2+) chelator 1, 2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA)-AM]. The activation of JNK by BAPTA-AM occurs despite a decrease in cytosolic Ca(2+) concentration as detected by the indicator dye fura 2, but appears to be related to Ca(2+) metabolism, because modification of BAPTA with two methyl groups increases not only the chelation affinity for Ca(2+), but also the potency for JNK activation. BAPTA-AM stimulates Ca(2+) influx across the plasma membrane, and the resulting local Ca(2+) increases are probably involved in activation of JNK because Ca(2+) influx inhibitors (SKF-96365, nifedipine) and lowering of the free extracellular Ca(2+) concentration with EGTA reduce the BAPTA-induced JNK activation.

adalat pill 2016-06-04

Acute renal failure (ARF) is a rare but severe complication of active idiopathic nephrotic syndrome (INS) in children. It may be due to several causes with different outcomes. Both the clinical picture of the patient as well as laboratory, imaging and histopathological findings may help in the diagnosis. We present a case of drug-induced acute interstitial nephritis (AIN), complicated with ARF, in a 2(1/2) -year-old girl with active INS. The child was referred to the Hippokration General Hospital, Thessaloniki, Greece hospital with steroid-resistant NS; renal biopsy was performed, which did not show any remarkable findings and cyclosporine was administered in addition to steroid therapy. The first day after biopsy, the child developed gross hematuria and abdominal pain and an antibiotic was added to her treatment. In the following days, fever, vomiting, hypertension and ARF occurred. Ultrasound study revealed enlarged kidneys with increased echogenity buy adalat online and loss of corticomedullary differentiation. The antibiotic and cyclosporine were stopped and the child was managed with furosemide, nifedipine and steroids. A second renal biopsy was performed, which confirmed the diagnosis of acute interstitial nephritis. The child did not require dialysis therapy. Her urine output improved gradually and the serum creatinine normalized one month after the initial episode. Our case re-emphasizes the need for investigation of factors precipitating ARF in children with idiopathic NS.

adalat retard dose 2017-09-21

Human mesangial cells were cultured in medium containing 5% fetal calf serum (FCS), with or without benidipine, or other calcium channel blockers for 20 h, and [(3)H]thymidine incorporation were measured. Analysis of cell cycle dependency was carried out, using platelet-derived buy adalat online growth factor as a competence factor, which transfers cells from the G0 to the G1 (G0/G1) phase, and insulin as a progression factor, which transfers cells from the G1 to the S (G1/S) phase. Cells were also analyzed by flow cytometry.

adalat 90 mg 2017-11-02

Antipsychotic drugs can modulate transcription factors and also nuclear receptors, but their action on glucocorticoid receptors (GR)-members of the steroid/thyroid hormone receptor family has not been studied so far. In the present study we investigated effects of various antipsychotics on the glucocorticoid-mediated gene transcription in fibroblast cells, stably transfected with a mouse mammary tumor virus promoter (LMCAT cells). Chlorpromazine (3-100 microM) inhibited the corticosterone-induced gene transcription in a concentration- and time-dependent manner. Clozapine showed a similar, but less potent effect, while haloperidol acted only in high concentrations, and other antipsychotic drugs (sulpiride, raclopride, remoxipride) were without any effect. It was also found that a phorbol ester (an activator of protein kinase C (PKC)) and A-23187 (Ca(2+)-ionophore) attenuated the inhibitory effect of chlorpromazine on the GR-induced gene transcription. An antagonist of the L-type Ca(2+) channel, as well as an inhibitor of phospholipase C (PLC) inhibited the corticosterone-induced gene transcription, but had no effect on the chlorpromazine-induced changes. The involvement of a PKC/PLC pathway in the chlorpromazine action was confirmed by Western blot analysis which showed that the drug in question decreased the PLC-beta(1) protein level, and to a lesser extent that of the PKC-alpha protein in LMCAT cells. The aforementioned data suggest that inhibition of the glucocorticosteroid-induced gene transcription by chlorpromazine and clozapine may be a mechanism by which these drugs block some effects induced by glucocorticoids. The inhibitory effect of chlorpromazine on the corticosterone-induced buy adalat online gene transcription seems to depend on the inhibition of Ca(2+) influx and/or the inhibition of some calcium-dependent enzymes, e.g. phospholipase beta(1).

adalat cc dosage 2016-08-17

Myasthenia gravis is an autoimmune disorder where antibodies against the nicotinic Ach receptor resulting in impaired transmission at the NM junction. A number of drugs have been reported to cause neuromuscular blockade and/or to increase weakness in myasthenia gravis. We report a case of myasthenia buy adalat online gravis in which the calcium channel blocker-nifedipine caused the worsening of the symptoms.

adalat y alcohol 2016-09-23

The transient outward current (ITO) in magnocellular neurosecretory cells was studied using whole cell patch clamp recordings made from supraoptic neurons acutely isolated from the adult rat. In the presence of tetrodotoxin, depolarizing steps applied from a negative holding potential evoked a rapidly activating and inactivating outward current followed by a slowly activating and sustained outward current. The ITO was unaffected by tetraethylammonium (TEA), but was blocked by 4-aminopyridine. The ITO evoked by depolarization from negative potentials in the presence of 40 mM TEA was not different from that revealed by digital subtraction of current traces recorded buy adalat online with and without a negative conditioning prepulse in control solutions. Tail current analysis during perfusion of media containing different external [K+] indicated that ITO is selective for K+ ions. Exposure to Ca(2+)-free solutions containing divalent inorganic cations such as Cd2+ and Ni2+ could cause shifts in voltage-dependency and, thereby, reduce the amplitude of ITO recorded at fixed submaximal potentials, The maximal ITO achievable under these conditions, however, was reduced compared to control. Moreover, the ITO was also reduced by application of organic Ca2+ channel antagonists such as nifedipine and omega-conotoxin GVIA, indicating that a component of the ITO is somehow dependent on Ca2+ influx.

adalat xl dosage 2016-03-24

Aspirin is strongly implicated in the pathogenesis of Reye's syndrome, a childhood disorder characterized by hyperammonemia, microvesicular steatosis, and encephalopathy. Previously, we showed that salicylate, the active metabolite of aspirin, induces the mitochondrial permeability transition (MPT) in isolated mitochondria, as do several other chemicals implicated in Reye's-related disorders. Opening of a high conductance, cyclosporin A-sensitive pore in the mitochondrial inner membrane causes the MPT, leading to swelling, depolarization, and uncoupling of oxidative phosphorylation. The goal of this study was to characterize the role of the MPT in salicylate toxicity to cultured rat hepatocytes. Salicylate (0.3-5 mM) caused concentration-dependent cell killing. In Krebs-Ringer buffer, half-maximal cell killing occurred 150 min after 3 mM salicylate. buy adalat online Increasing Ca2+ enhanced salicylate lethality. Salicylate-dependent cell killing was blocked by 0.5-5 microM cyclosporin A and its nonimmunosuppresive analog, 4-methylvaline cyclosporin, implicating the MPT in the pathogenesis of cell killing. The contribution of the MPT to lethal cell injury was confirmed by laser scanning confocal microscopy, which demonstrated the redistribution of the fluorophore calcein from the cytosol into mitochondria prior to cell killing, an event blocked by cyclosporin A. Salicylate toxicity was enhanced at high extracellular Ca2+. In the range of 10-100 microM, several chemically diverse calcium antagonists blocked or reduced salicylate toxicity including verapamil, diltiazem, chlorpromazine, nifedipine, and nisoldipine. Calcium antagonists also blocked the increase of mitochondrial free Ca2+ in high Ca2+ buffer, as determined by confocal imaging of the fluorophore Rhod-2. These data with salicylate suggest that onset of the MPT may be the common pathophysiologic mechanism causing mitochondrial injury in Reye's syndrome and Reye's-related drug toxicities. Further, elevated intramitochondrial Ca2+ may be a predisposing condition promoting onset of the MPT by Reye's-related chemicals.

adalat cc medication 2015-03-13

From the results of the screening tests of hypromellose solution, 1.0% hypromellose was chosen as the vehicle for nifedipine enteral suspensions, made from both crushed tablets and nifedipine powder. Nifedipine suspensions made from hypromellose 1.0% were easiest to Sustiva Cost redisperse as a homogenous solution, and it also appeared best on visual inspection. The content uniformity of the suspension complied with the test recommended by the European Pharmacopoeia. The 1.0% hypromellose solution was found to be microbiologically stable for 6 months and physically stable for 12 months.

tab adalat r 2017-06-09

The thromboxane A2 (TXA2) mimetic U44069 has been demonstrated to reduce the GFR and filtration fraction of the normal isolated perfused rat kidney markedly, suggesting a predominant constriction of preglomerular vessels Prednisone 100 Mg . To assess this possibility directly, effects of U44069 on the renal microvessels of the isolated perfused hydronephrotic kidney were examined. At 10(-6) mol/L, U44069 elicited a 27 +/- 2% decrease in afferent arteriolar (AA) diameter (from 18.8 +/- 0.3 to 13.7 +/- 0.3 micron, P < 0.001). In contrast, efferent arteriolar (EA) diameter decreased by only 9 +/- 1% (from 16.4 +/- 0.5 to 15.0 +/- 0.5 micron, P < 0.001). These effects on both AA and EA were completely reversed by the TXA2 receptor antagonist SQ29548. The calcium antagonist diltiazem reversed U44069-induced AA constriction by 83 +/- 5%. The U44069-induced EA constriction was insensitive to the vasodilator action of diltiazem at concentrations from 10(-8) to 10(-6) mol/L, but at 10(-5) mol/L, diltiazem increased the EA diameter significantly, albeit modestly. Nifedipine also reversed the U44069-induced AA constriction (81 +/- 7%), but failed to inhibit the EA constriction at concentrations from 10(-9) to 10(-6) mol/L. These findings constitute the first direct evidence that a TXA2 agonist preferentially constricts the afferent arteriole. Furthermore, the ability of both the calcium antagonist and SQ29548 to reverse the renal microvascular actions of TXA2 agonists suggests a potential utility of these agents in ameliorating TXA2-induced renal hemodynamic abnormalities.

adalat medicine 2016-06-20

The results show that the elevation in [Ca2+]i of the PMNLs is associated with down-regulation of the mRNA of their Fc gamma RIII receptors, which is at least, in part, responsible for the impaired phagocytosis. These derangements in the metabolism and function of the PMNLs are most likely Levaquin Overdose responsible for the increased susceptibility of the diabetic patients to infection. Calcium channel blockers may be a beneficial adjunct therapy in patients with uncontrolled diabetes.

adalat generic 2016-03-13

Ninety women were randomised: 44 to nifedipine and 46 to terbutaline. Initial ECV success rate was 15/44 (34.1%) versus 24/46 (52.2%) (relative risk [RR] 0.7, 95% CI 0.4-1.1; P= 0.094), and caesarean delivery rate was 34/44 (77.3%) versus 26/46 (56.5%) (RR 1.4, 95% CI 1.01-1.85; numbers needed to treat to benefit 5, 95% CI Topamax High Dosage 2.5-55; P= 0.046) for nifedipine and terbutaline groups, respectively. Neonatal outcome was not different.

adalat drug 2017-12-17

Imidapril is a Plavix Drug Class well tolerated ACE inhibitor that has been shown to be as efficacious as sustained-release nifedipine in the treatment of hypertension and left ventricular hypertrophy in patients with previously untreated hypertension.

adalat xl dose 2017-03-14

Today the management of resistant hypertension is a critical health problem: the main difficulty on this field is the discrimination of cases of poor therapeutic adherence from cases of real resistance. This gives rise to the need of high throughput and reliable quantification methods for the Therapeutic Drug Monitoring (TDM) of antihypertensive drugs. The aim of this work was the development and validation of a UHPLC-Tandem mass spectrometry assay for this application and its use in plasma from patients with resistant hypertension. The novelty of this method resides in the ability to simultaneously quantify a wide panel of antihypertensive drugs: amlodipine, atenolol, clonidine, chlortalidone, doxazosin, hydrochlorothiazide, nifedipine, olmesartan, ramipril and telmisartan. Moreover, this method stands out for its simplicity and cheapness, resulting feasible for clinical routine. Both standards and quality controls were prepared in human plasma. After the addition of internal standard, each sample underwent protein precipitation with acetonitrile and was then dried. Extracts were resuspended in water:acetonitrile 90:10 (0.05% formic acid) and then injected into the chromatographic system. Chromatographic separation was performed on an Acquity(®) UPLC HSS T3 1.8μm 2.1×150mm column, with a gradient of water and acetonitrile, both added with 0.05% formic acid. Accuracy, intra-day and inter-day precision fitted FDA guidelines for all analytes, while matrix effects and recoveries resulted stable between samples for each analyte. Finally, we tested this method by monitoring plasma concentrations in 22 hypertensive patients with good Altace Drug Generic results. This simple analytical method could represent a useful tool for the management of antihypertensive therapy.

adalat reviews 2016-02-20

Alkyl ester analogues of nifedipine, in which the ortho-nitrophenyl group at position 4 is replaced by 2-methylthio-1-phenylamino-5-imidazolyl substituent, were synthesized and evaluated as calcium-channel antagonists using the high K(+) contraction of guinea-pig ileal longitudinal smooth muscle. The results for the symmetrical esters showed that in the series of alkyl esters increasing the length of methylene chain in C-3 and C-5 ester substituents for more than two methylene units decreases activity. In the phenylalkyl ester series increasing the length of methylene chain also decreases activity. The results demonstrate that most of the compounds had similar activity to the reference drug nifedipine. In addition, two compounds, 5b and 5f Aricept 10 Mg were more active than the nifedipine.

adalat xl dosing 2016-10-23

A group of dialkyl and diarylester analogues of nifedipine, in which the ortho-nitrophenyl group at position 4 was replaced by a 1-methyl-4,5-dichloroimidazolyl substituent, were synthesized and evaluated as calcium-channel antagonists using the high K(+)concentration of guinea-pig ileum longitudinal smooth muscle. The structure of all compounds was confirmed by IR,(1)H-NMR, and mass spectra. The calcium-channel antagonist activity of compounds 10a-f demonstrated that compound Crestor Generic Alternative 10b was the most active and 10f the least active one. With unsymmetrical diesters 12a-k, the most active compound was the ethyl, phenethyl derivative. Structural parameters on the calcium-channel antagonist activity were evaluated by QSAR analysis and a linear correlation was found between the -log IC(50) values of these compounds and their constitutional and topological properties.

adalat medication 2015-08-13

Both DIDS and NFA could inhibit the thrombin (1 Celexa 200 Mg U/ml) induced PAG in a dose-dependent manner, whereas had little effect on resting [Ca2+]i. As compared with the control group, DIDS, SK&F96365 and Nifedipine could significantly reduce the PAG, Ca2+ release and Ca2+ influx in thrombin activated platelet (P < 0.05). The combination of DIDS and SK&F96365 had greater effects in reducing the PAG, Ca2+ release and Ca2+ influx than either reagent alone (P < 0.05). The combination of DIDS and nifedipine also had greater effect than each alone in reducing Ca2+ release (P < 0.05). The combination of NFA and SK&F96365 weakened each other's effect on Ca2+ release (P < 0.05), while NFA and nifedipine weakened each other's effects on PAG, Ca2+ release and Ca2+ influx in thrombin activated platelet (P < 0.05).

adalat medication nifedipine 2016-10-24

In our recent study, we found that the Ca(2+) antagonist, nilvadipine caused significant preservation of photoreceptor cells in The Royal College of Surgeons (RCS) rats [Invest. Ophthalmol. Vis. Sci. 43 (2002) 919]. Here, to elucidate the mechanisms of nilvadipine- Nexium 50 Mg induced effects we analyzed altered gene expression of 1101 genes commonly expressed in rodent by DNA microarray analysis in the retinas of nilvadipine-treated and untreated RCS rats and SD rat. In the total number of genes, the expression of 30 genes was altered upon administration of nilvadipine to RCS rats, including several genes related to the apoptotic pathway and other mechanisms. Remarkably, neurotrophic factors, FGF-2 and Arc, known to suppress the apoptosis in the central nervous system, were up-regulated. These changes were also confirmed by real-time quantitative (Taqman) RT-PCR and Western blot analysis. Therefore, our present data suggested that administration of nilvadipine to RCS rats increases the expression of endogenous FGF-2 and Arc in retina, and potentially has a protective effect against retinal degeneration.

adalat 50 mg 2017-07-30

Current results suggest that the aqueous extract used in this study possess antihypertensive activity against ethanol and sucrose induced hypertension in rats by the improvement of biochemical and oxidative status, and by protecting Casodex Generic Bicalutamide liver, kidney and vascular endothelium against damages induced by chronic consumption of ethanol and sucrose.