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Micronase (Glyburide)

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Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Other names for this medication:

Similar Products:
Glucophage, Actos, Glucotrol, Avandia


Also known as:  Glyburide.


Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Generic Micronase is a sulfonylurea antidiabetic medicine. It works by causing the pancreas to release insulin, which helps to lower blood sugar.

Brand name of Generic Micronase is Micronase.


Take Generic Micronase by mouth with food.

If you are taking 1 dose daily, take Generic Micronase with breakfast or the first main meal of the day unless your doctor tells you otherwise.

High amounts of dietary fiber may decrease Generic Micronase 's effectiveness, resulting in high blood sugar.

Generic Micronase works best if it is taken at the same time each day.

Continue to take Generic Micronase even if you feel well.

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


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


Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children.

Side effects

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

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

Do not take Generic Micronase if you have certain severe problems associated with diabetes (eg, diabetic ketoacidosis, diabetic coma).

Do not take Generic Micronase if you have moderate to severe burns or very high blood acid levels (acidosis) you are taking bosentan.

Do not take Generic Micronase if you are taking bosentan.

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

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

Be careful with Generic Micronase if you have had a severe allergic reaction (eg, a severe rash, hives, itching, breathing difficulties, dizziness) to any other sulfonamide medicine, such as acetazolamide, celecoxib, certain diuretics (eg, hydrochlorothiazide), glipizide, probenecid, sulfamethoxazole, valdecoxib, or zonisamide.

Be careful with Generic Micronase if you have a history of liver, kidney, thyroid, or heart problems.

Be careful with Generic Micronase if you have stomach or bowel problems (eg, stomach or bowel blockage, stomach paralysis), drink alcohol, or have had poor nutrition.

Be careful with Generic Micronase if you have type 1 diabetes, very poor health, a high fever, a severe infection, severe diarrhea, or high blood acid levels, or have had a severe injury.

Be careful with Generic Micronase if you have a history of certain hormonal problems (eg, adrenal or pituitary problems, syndrome of inappropriate secretion of antidiuretic hormone [SIADH]), low blood sodium levels, anemia, or glucose-6-phosphate dehydrogenase (G6PD) deficiency.

Be careful with Generic Micronase if you will be having surgery.

Be careful with Generic Micronase if you are taking bosentan because liver problems may occur; the effectiveness of both medicines may be decreased; beta-blockers (eg, propranolol) because the risk of low blood sugar may be increased; they may also hide certain signs of low blood sugar and make it more difficult to notice; angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril), anticoagulants (eg, warfarin), azole antifungals (eg, miconazole, ketoconazole), chloramphenicol, clarithromycin, clofibrate, fenfluramine, insulin, monoamine oxidase inhibitors (MAOIs) (eg, phenelzine), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), phenylbutazone, probenecid, quinolone antibiotics (eg, ciprofloxacin), salicylates (eg, aspirin), or sulfonamides (eg, sulfamethoxazole) because the risk of low blood sugar may be increased; calcium channel blockers (eg, diltiazem), corticosteroids (eg, prednisone), decongestants (eg, pseudoephedrine), diazoxide, diuretics (eg, furosemide, hydrochlorothiazide), estrogens, hormonal contraceptives (eg, birth control pills), isoniazid, niacin, phenothiazines (eg, promethazine), phenytoin, rifamycins (eg, rifampin), sympathomimetics (eg, albuterol, epinephrine, terbutaline), or thyroid supplements (eg, levothyroxine) because they may decrease Generic Micronase 's effectiveness, resulting in high blood sugar; gemfibrozil because blood sugar may be increased or decreased; cyclosporine because the risk of its side effects may be increased by Generic Micronase.

Avoid alcohol.

Do not stop taking Generic Micronase suddenly.

micronase drug interactions

ATP-sensitive K+ (K(ATP)) channels were reported to be involved in morphine analgesia in vivo. The present study, using patch-clamp technique in brain slices of neonatal (P12-P16) and adult rats, investigated cellular actions of K(ATP) channel ligands and their interactions with morphine in the ventrolateral periaqueductal gray (PAG), a crucial site for morphine analgesia. In neonatal PAG neurons, morphine depressed evoked inhibitory postsynaptic currents (IPSCs) in almost all tested neurons and elicited an inwardly rectifying K+ current in one-third of tested neurons. Glibenclamide (1-10 microM), a K(ATP) channel blocker, did not affect the membrane current or synaptic current per se but also failed to affect the effects of morphine. No outward current was elicited upon using microelectrodes containing ATP-free internal solution. In adult neurons, morphine, at the concentration up to 300 microM, failed to activate K+ current in all 25 neurons tested but depressed IPSCs to a comparable extent as that in neonatal neurons. Glibenclamide also failed to alter the effect of morphine in adult neurons. The openers of K(ATP) channels, lemakalim (10-30 microM) and diazoxide (10-500 microM), unlike morphine, did not increase membrane currents in both neonatal and adult neurons. However, diazoxide induced a glibenclamide-sensitive outward current in hippocampal CA1 neurons. It is concluded that K(ATP) channels display little functional role per se and might not be involved in effects of morphine in the ventrolateral PAG. The correlation between the insensitivity in K+ channel activation and the less antinociceptive response to morphine in adults was discussed.

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The aim was to investigate the properties of two potassium channel openers in human myometrium.

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Study one: There was no significant difference in mRNA expression levels of SUR1, SUR2, and Kir6.2 in heart between diabetic, insulin-treated diabetic and control groups (P > 0.05). Study two: Glibenclamide-treated non-diabetic rats had higher mRNA expression levels of SUR1 and SUR2 in heart than normal control. The SUR1 were 43.0 +/- 16.6 vs 30.8 +/- 7.8 (P < 0.05), SUR2 161.9 +/- 51.0 vs 118.9 +/- 40.9 (P < 0.05), respectively. No difference in heart Kir6.2 mRNA level was found between the two groups (P > 0.05). Comparison between Glibenclamide-treated diabetic and non-treated diabetic rats showed that there was no change in mRNA levels of SUR1, SUR2 and Kir6.2 in heart (P > 0.05).

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Magnesium depletion induces K+ and Na+ uniports in rat liver mitochondria. The purpose of the present study was to investigate the effects exerted by the antidiabetic sulfonylurea, glibenclamide, a well known blocker of ATP-sensitive potassium channels, on mitochondrial K+ and Na+ uniports. The K+ and Na+ uniport activities were monitored indirectly, in energized mitochondria, by following K+ and Na+ influxes as measured by light scattering. The membrane potential of the mitochondria was determined using a TPP+ selective electrode. Equilibrium binding measurements of glibenclamide to the inner mitochondrial membrane was performed with [3H]glibenclamide. Mitochondrial K+ and Na+ uniports were found to be inhibited by glibenclamide in a concentration-dependent manner, with IC50 of 20 +/- 7 and 15 +/- 8 microM, respectively. On lowering of the pH value, the potency of glibenclamide to inhibit the uniports activity was increased. Binding studies revealed the presence of a single class of low affinity binding sites for glibenclamide in the inner mitochondrial membrane, with a Kd of 4 +/- 2 microM and a BMAX of 148 +/- 50 pmoles/mg of protein. The present study provides evidence that both mitochondrial K+ and Na+ uniport activities are sensitive to the antidiabetic sulfonylurea, glibenclamide.

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This study addressed the possibility that acetylcholine-induced relaxation in the rabbit aorta is mediated by dual mechanisms: one N omega-nitro-L-arginine (NLA)-sensitive, the other glybenclamide-sensitive. Acetylcholine, nitroglycerin and BRL38227 (lemakalim), an activator of glybenclamide-sensitive potassium channels, were added to an organ bath containing rabbit aortic rings in a cumulative manner in the absence or presence of NLA and/or glybenclamide. NLA inhibited acetylcholine-induced relaxation and potentiated the relaxant response to nitroglycerin. BRL38227 caused a dose-dependent relaxation in rabbit aortic rings, and 30 microM glybenclamide produced essentially complete inhibition of this relaxation. Glybenclamide alone produced no inhibition of acetylcholine-induced relaxation. These results indicate that glybenclamide-sensitive potassium channels in the rabbit aorta play no role in mediating the relaxant response to acetylcholine, while NLA can produce a selective and essentially complete blockade of the relaxant response to acetylcholine in the rabbit aorta.

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Compared to the currently available therapeutic drugs for peripheral vascular diseases, agents that are selective for relaxing pulmonary circulation are scarce. The present study was undertaken, using isometric tension change measurement and whole-cell patch-clamp electrophysiology methods, to evaluate the vascular relaxation effect and the underlying mechanisms involved of two naturally found alkaloids: paeonol (2-hydroxy-4-methoxy-acetophenone), acetovanillone (4-hydroxy-3-methoxy-acetophenone) and the non-substituted analogue acetophenone on pulmonary artery of Sprague-Dawley rats. Cumulative administration (3 microM-1 mM) of acetophenone analogues resulted in a concentration-dependent relaxation of phenylephrine (1 microM) pre-contracted pulmonary artery. A relative order of inhibitory potency, estimated by comparing the concentration at which a 50% relaxation of phenylephrine-induced contraction observed was: acetovanillone > paeonol > acetophenone. Endothelial denudation and inhibition of nitric oxide synthase (with 20 microM N(G)-nitro-L-arginine methyl-ester) only moderately suppressed (17.6 +/- 4.2%) acetovanillone- but not paeonol- or acetophenone-mediated maximum relaxation. Glibenclamide (3 microM, an ATP-sensitive K(+) (IK(ATP)) channel blocker) markedly attenuated all acetophenone analogues-mediated endothelium-independent relaxation. Neither cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL 12330A, 10 microM), iberiotoxin (300 nM), 4-aminopyridine (3 mM), (+/-)-propranolol (1 microM, a non-selective beta-adrenoceptor blocker) nor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) (3 microM, a guanylate cyclase inhibitor) altered endothelium-independent relaxation. In electrophysiological experiments using single pulmonary artery smooth muscle cells, acetovanillone, paeonol, acetophenone and cromakalim activated glibenclamide-sensitive, IK(ATP) channels. In conclusion, our results demonstrate that acetophenone analogues caused pulmonary artery relaxation through opening of IK(ATP) channels. In addition, acetovanillone-mediated pulmonary artery relaxation is partly depended on nitric oxide released from endothelium.

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Glibenclamide's effects on agonist-induced constrictions are unlikely to be via an inhibition of ATP-sensitive K+ channels, and with U46619- and U44069-induced constrictions, glibenclamide may be acting as a competitive antagonist of thromboxane receptors.

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In a clinical trial with patients with chronic heart failure, a higher incidence of elevated levels of liver transaminases was observed during concomitant treatment with bosentan, a dual endothelin receptor antagonist, and glyburide (INN, glibenclamide), a sulfonylurea-type antidiabetic drug, than with treatment with bosentan alone. This study was conducted to investigate a possible pharmacokinetic interaction between bosentan and glyburide.

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A novel pyranoquinoline analog (BMS-188107) of the ATP-sensitive potassium channel (KATP) opener cromakalim was previously shown to be devoid of KATP opening activity in nonischemic myocardium and vascular smooth muscle, but appeared to be a relatively potent calcium antagonist. This clear differentiation between channels within a structural series is a novel finding. With the idea that KATP openers are often more active in ischemic relative to nonischemic myocardium, we determined the cardioprotective effects of this agent in isolated rat hearts and whether these anti-ischemic effects are abolished by KATP blockade. Isolated rat hearts were subjected to 25 min of global ischemia and 30 min of reperfusion and the severity of ischemic/reperfusion injury was determined. BMS-188107 was given before ischemia at 0.5 to 10 microM. Pretreatment (before ischemia) with BMS-188107 caused significant cardiodepressant activity and increased coronary flow only at a concentration of 10 microM, although modest negative inotropic effects were observed at the 0.5 and 1 microM concentrations. Significant improvements in postischemic contractile function and reductions in lactate dehydrogenase release were observed with 1 to 10 microM BMS-188107, indicating significant reductions in ischemic/reperfusion injury. Neither the pre- nor the postischemic effects of 1 to 10 microM BMS-188107 were significantly altered by the KATP blockers sodium 5-hydroxydecanoate (100 microM) or glyburide (1 microM). Previous studies did not determine the effect of BMS-188107 on sodium channels and thus, the effect of this agent on maximum upstroke velocity of the action potential was determined.(ABSTRACT TRUNCATED AT 250 WORDS)

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Erythrocytes release ATP in response to exposure to the physiological stimulus of lowered oxygen (O(2)) tension as well as pharmacological activation of the prostacyclin receptor (IPR). ATP release in response to these stimuli requires activation of adenylyl cyclase, accumulation of cAMP, and activation of protein kinase A. The mechanism by which ATP, a highly charged anion, exits the erythrocyte in response to lowered O(2) tension or receptor-mediated IPR activation by iloprost is unknown. It was demonstrated previously that inhibiting pannexin 1 with carbenoxolone inhibits hypotonically induced ATP release from human erythrocytes. Here we demonstrate that three structurally dissimilar compounds known to inhibit pannexin 1 prevent ATP release in response to lowered O(2) tension but not to iloprost-induced ATP release. These results suggest that pannexin 1 is the conduit for ATP release from erythrocytes in response to lowered O(2) tension. However, the identity of the conduit for iloprost-induced ATP release remains unknown.

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An estimated 20 million Americans suffer from diabetes. Patients with non-insulin-dependent diabetes mellitus (NIDDM) comprise approximately 90% of the diabetic population. An estimated 10-30% of patients with NIDDM withdraw from their prescribed regimen within 1 year of diagnosis, and of the remainder, nearly 20% administer insufficient medication to facilitate an adequate reduction in blood glucose. A randomized trial was undertaken to discern the effect of pharmacy-based value-added utilities on prescription-refill compliance with sulfonylurea therapy and health service utilization. The subjects were 258 Medicaid beneficiaries from the state of South Carolina, previously untreated for NIDDM, prescribed 5 mg of the second-generation sulfonylurea glyburide twice daily, and monitored with regard to prescription-refill compliance and health service utilization for 1 year. Subjects provided informed consent and were randomly assigned to one of four experimental groups: (i) the control cohort received standard pharmaceutical care with each dispensing of glyburide; (ii) the second cohort received standard pharmaceutical care and was mailed a medication-refill reminder 10 days prior to each sequential refill date; (iii) the third cohort received standard pharmaceutical care and was provided unit-of-use packaging with each prescription-refill request; (iv) the fourth cohort received standard pharmaceutical care, mailed medication-refill reminders, and unit-of-use packaging. Analysis of variance (ANOVA) procedures revealed that patients receiving mailed prescription-refill reminders, unit-of-use packaging, or a combination of both interventions achieved a significant (P < or = 0.05) increase in the Medication Possession Ratio (MPR) for sulfonylurea therapy relative to controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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We expanded and verified our previously published pregnancy PBPK model by incorporating hepatic CYP2B6 induction (based on in vitro data), CYP2C9 induction (based on phenytoin PK) and CYP2C19 suppression (based on proguanil PK), into the model. This model accounted for gestational age-dependent changes in maternal physiology and hepatic CYP3A, CYP1A2 and CYP2D6 activity. For verification, the pregnancy-related changes in the disposition of methadone (cleared by CYP2B6, 3A and 2C19) and glyburide (cleared by CYP3A, 2C9 and 2C19) were predicted.

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Extracts of pine needles (Pinus densiflora Sieb. et Zucc.) have diverse physiological and pharmacological actions. In this study we show that pine needle extract alters pacemaker currents in interstitial cells of Cajal (ICC) by modulating ATP-sensitive K+ channels and that this effect is mediated by prostaglandins. In whole cell patches at 30 degrees , ICC generated spontaneous pacemaker potentials in the current clamp mode (I = 0), and inward currents (pacemaker currents) in the voltage clamp mode at a holding potential of -70 mV. Pine needle extract hyperpolarized the membrane potential, and in voltage clamp mode decreased both the frequency and amplitude of the pacemaker currents, and increased the resting currents in the outward direction. It also inhibited the pacemaker currents in a dose-dependent manner. Because the effects of pine needle extract on pacemaker currents were the same as those of pinacidil (an ATP-sensitive K+ channel opener) we tested the effect of glibenclamide (an ATP-sensitive K+ channels blocker) on ICC exposed to pine needle extract. The effects of pine needle extract on pacemaker currents were blocked by glibenclamide. To see whether production of prostaglandins (PGs) is involved in the inhibitory effect of pine needle extract on pacemaker currents, we tested the effects of naproxen, a non-selective cyclooxygenase (COX-1 and COX-2) inhibitor, and AH6809, a prostaglandin EP1 and EP2 receptor antagonist. Naproxen and AH6809 blocked the inhibitory effects of pine needle extract on ICC. These results indicate that pine needle extract inhibits the pacemaker currents of ICC by activating ATP-sensitive K+ channels via the production of PGs.

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This study examines the effect of rosiglitazone on urinary albumin excretion (UAE) in patients with type II diabetes. Urinary albumin: creatinine ratio (ACR) was measured in a 52-week, open-label, cardiac safety study comparing rosiglitazone and glyburide. Patients were randomised to treatment with rosiglitazone 4 mg b.i.d. or glyburide. ACR was measured at baseline and after 28 and 52 weeks of treatment. Statistically significant reductions from baseline in ACR were observed in both treatment groups at week 28. By week 52, only the rosiglitazone group showed a significant reduction from baseline. Similar results were observed for the overall study population and for the subset of patients with baseline microalbuminuria. For patients with microalbuminuria at baseline, reductions in ACR did not correlate strongly with reductions in glycosylated haemoglobin, or fasting plasma glucose, but showed strong correlation with changes in mean 24-h systolic and diastolic blood pressure for rosiglitazone-treated patients (deltaACR vs deltamean 24-h systolic blood pressure, r=0.875; deltaACR vs deltamean 24-h diastolic blood pressure, r=0.755; P < 0.05 for both). No such correlation was observed for glyburide-treated patients. In conclusion, rosiglitazone treatment was associated with a decrease in urinary albumin excretion. These findings suggest a potential beneficial effect of rosiglitazone in the treatment or prevention of renal and vascular complications of type II diabetes.

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Enterostatin (10(-9) to 10(-5) M) inhibited insulin secretion from islets incubated in the presence of 16.7 mM glucose in a dose-dependent manner. Enterostatin also inhibited insulin secretion stimulated by glybenclamide (5.0 and 10 microM), phorbol 12-myristate-13-acetate (TPA) (50 and 100 nM), and the kappa-opioid agonist U50,488 (100 nM). The inhibitory effect of enterostatin on TPA-induced insulin secretion was attenuated but still remained in the absence of extracellular Ca2+. The enterostatin inhibition of insulin secretion was blocked by 8-Br-cAMP (1 mM) independent of extracellular Ca2+. Enterostatin reduced the increase in intracellular cyclic AMP (cAMP) content produced by U50,488 (100 nM) and the changes in cAMP content were parallel with changes in insulin release.

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We have recently proposed that opening of mitochondrial K(ATP) channels (mitoK(ATP)) acts as a trigger for preconditioning (PC) by causing mitochondria to produce reactive oxygen species (ROS). Controversy exists as to whether the putative sarcolemma-selective K(ATP) channel opener P1075 also opens mitoK(ATP) channels and may be cardioprotective. We purified mitoK(ATP) channels from either rabbit heart, rat heart or rat brain and reconstituted the proteins into liposomes. mitoK(ATP) channels from each of these tissues were opened by P1075 with EC(50) values of 60-90 nM. We next tested whether P1075 causes rabbit cardiomyocytes to produce ROS in a K(ATP)-dependent fashion. Mitochondrial ROS production was monitored by the appearance of fluorescence as reduced MitoTracker Red was oxidized. P1075 (100 microM) led to a 44 +/- 9% increase in ROS generation (P < 0.001 vs. untreated cells), which was similar to the increase seen with 50 microM diazoxide, a selective mitoK(ATP) channel opener (49 +/- 9%, P < 0.001 vs. untreated cells). The effect of P1075 was equally potent at a concentration of 150 nM. The P1075-induced increase in ROS production was blocked by 50 microM glibenclamide (GLI), a non-selective K(ATP) blocker, and by 5-hydroxydecanoate (1 mM), a highly selective mitoK(ATP) blocker (-6 +/- 14% and +4 +/- 12%, respectively; P = n.s). In isolated rabbit hearts, P1075 (150 nM) markedly reduced infarct size compared to control animals (10.6 +/- 8.1% of the area at risk vs. 31.5 +/- 5.6%, P < 0.05). GLI (5 microM) as well as 5-hydroxydecanoate (200 microM) completely blocked P1075's anti-infarct effect (31.7 +/- 9.5% and 27.7 +/- 4.6% infarction, respectively; P = n.s. vs. untreated hearts). These data provide strong evidence that P1075 does open mitoK(ATP) channels and protects the ischemic rabbit heart in a mitoK(ATP)-dependent manner.

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The objective of this study was to assess the effects of ischemic preconditioning (IP) on hydroxyl free radical production in an in vivo rabbit model of regional ischemia and reperfusion. Another goal was to determine whether K(ATP) channels are involved in these effects. The hearts of anesthetized and mechanically ventilated New Zealand White rabbits were exposed through a left thoracotomy. After i.v. salicylate (100 mg/kg) administration, all animals underwent a 30-min stabilization period followed by 40 min of regional ischemia and 2 h of reperfusion. In the IP group, IP was elicited by 5 min of ischemia followed by 10 min of reperfusion (prior to the 40-min ischemia period). Glibenclamide, a K(ATP) channel blocker, was administered prior to the preconditioning stimulus. Infarct size was measured by 2,3,5-triphenyl tetrazolium chloride (TTC) staining. We quantified the hydroxyl-mediated conversion of salicylate to its 2,3 and 2,5-dihydroxybenzoate derivatives during reperfusion by high performance liquid chromatography coupled with electro-chemical detection.IP was evidenced by reduced infarct size compared to control animals: 22% vs. 58%, respectively. Glibenclamide inhibited this cardioprotective effect and infarct size was 53%. IP limited the increase in 2,3 and 2,5-dihydroxybenzoic acid to 24.3 and 23.8% above baseline, respectively. Glibenclamide abrogated this effect and the increase in 2,3 and 2,5-dihydroxybenzoic acid was 94.3 and 85% above baseline levels, respectively, similar to the increase in the control group. We demonstrated that IP decreased the formation of hydroxyl radicals during reperfusion. The fact that glibenclamide inhibited this effect, indicates that K(ATP) channels play a key role in this cardioprotective effect of IP.

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In this study, patch-clamp techniques were applied to cultured neonatal mouse cardiac myocytes (NMCM) to assess the contribution of cAMP stimulation to the anion permeability in this cell model. Addition of either isoproterenol or a cocktail to raise intracellular cAMP increased the whole cell currents of NMCM. The cAMP-dependent conductance was largely anionic, as determined under asymmetrical (low intracellular) Cl(-) conditions and symmetrical Cl(-) in the presence of various counterions, including Na(+), Mg(2+), Cs(+), and N-methyl-D-glucamine. Furthermore, the cAMP-stimulated conductance was also permeable to ATP. The cAMP-activated currents were inhibited by diphenylamine-2-carboxylate, glibenclamide, and an anti-cystic fibrosis transmembrane conductance regulator (CFTR) monoclonal antibody. The anti-CFTR monoclonal antibody failed, however, to inhibit an osmotically activated anion conductance, indicating that CFTR is not linked to osmotically stimulated currents in this cell model. Immunodetection studies of both neonatal mouse heart tissue and cultured NMCM revealed that CFTR is expressed in these preparations. The implication of CFTR in the cAMP-stimulated Cl(-)- and ATP-permeable conductance was further verified with NMCM of CFTR knockout mice [cftr(-/-)] in which cAMP stimulation was without effect on the whole cell currents. In addition, stimulation with protein kinase A and ATP induced Cl(-)-permeable single-channel activity in excised, inside-out patches from control, but not cftr(-/-) NMCM. The data in this report indicate that cAMP stimulation of NMCM activates an anion-permeable conductance with functional properties similar to those expected for CFTR, thus suggesting that CFTR may be responsible for the cAMP-activated conductance. CFTR may thus contribute to the permeation and/or regulation of Cl(-)- and ATP-permeable pathways in the developing heart.

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Particle size reduction is a suitable method to enhance the bioavailability of poorly soluble drugs. The reduction effectiveness depends on compound properties like crystallinity, hardness and morphology. Sometimes, it is difficult to obtain small particles. To solve this problem a combinative method was developed: a combination of freeze drying with high pressure homogenization (so-called H 96 process). The freeze drying modifies the drug structure to obtain a brittle, fragile starting material for the subsequent homogenization step. Screening experiments with glibenclamide have shown a relation between the lyophilization conditions and the final particle size. Systematic investigations using design of experiment (DoE) were conducted to identify optimal process parameters. The influence of the independent variables drug concentration and organic solvent composition during freeze drying were tested by conducting a two factorial design of experiment. The model drug was dissolved in mixtures of dimethyl sulfoxide (DMSO) and tert-butanol (TBA) in different concentrations, freeze dried and subsequently homogenized at high pressure. Using optimized process conditions the particle size after 20 cycles was very small: 164 nm (z-average) and 0.114 μm (d50%). On the contrary, with unmodified drug the results were 772 nm (z-average) and 2.686 μm (d50%). It was shown, that the structure modification of the drug by means of freeze drying can significantly improve the particle size reduction effectiveness of high pressure homogenization. The study confirmed also the usefulness of DoE for nanocrystal production.

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Bosentan caused dose-dependent and reversible liver injury in 2% to 18% of patients and caused a significant increase of serum bile salt levels (P <.01). Concomitant administration of glyburide (INN, glibenclamide) enhanced the cholestatic potency of bosentan. Similar effects were seen in rats, in which serum bile salt levels were increased by glyburide less than by bosentan, which increased the levels less than a combination of bosentan and glyburide. In vitro, Bsep-mediated taurocholate transport was inhibited by bosentan (inhibition constant, approximately 12 micromol/L) and metabolites (inhibition constant, approximately 8.5 micromol/L for metabolite Ro 47-8634).

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micronase 10 mg 2015-10-07

Almost three out of buy micronase online ten patients with a total attachment to the pharmacological treatment have chances of being controlled.

micronase cost 2015-02-14

This study evaluates for the first time the pharmacokinetics of oral Gb in children and constitutes a first step buy micronase online towards dose individualization of this drug in a particularly vulnerable population.

micronase 5 mg 2017-01-21

Both pioglitazone and glibenclamide improved glycemic control. Pioglitazone reduced fasting plasma insulin, whereas glibenclamide increased it. Pioglitazone increased the glucose infusion rate compared with glibenclamide. Pioglitazone, but not glibenclamide, improved the lipid profile, and, when rosuvastatin was added, there was a greater improvement with pioglitazone and rosuvastatin. Adiponectin was increased by pioglitazone (+0.5 μg/ml), with a further increase (+0.4 μg/ml) when rosuvastatin was added. A significant decrease in leptin (-3.1 ng/ml) and interleukin-6 (-0.4 pg/ml) was found only with pioglitazone; a similar trend (- buy micronase online 2.5 ng/ml and -0.3 pg/ml, respectively) was maintained after the addition of rosuvastatin.Rosuvastatin+pioglitazone decreased tumor necrosis factor-α (-0.3 ng/ml) and were superior to glibenclamide+rosuvastatin in reducing high-sensitivity C-reactive protein (-0.4 mg/l).Pioglitazone decreased ultrasound parameters, and the addition of rosuvastatin further decreased them both compared with randomization and glibenclamide.

dosage of micronase 2015-08-05

In the present study, the effects of cromakalim on tension and 86Rb+ efflux rate were evaluated in strips of dog and rat mesenteric arteries and compared with the variables obtained from ATP-depleted strips of both species. The cromakalim-induced relaxation was competitively antagonized by glibenclamide, with similar pA2 values, in both dog and rat mesenteric arteries. Glibenclamide caused an enhancement of the precontraction or a reversal of the cromakalim-induced inhibition in the mesenteric arteries of both species when cromakalim was applied prior to or during phenylephrine-contraction. The 86Rb+ efflux rate from the mesenteric arteries was significantly increased in both species after application of cromakalin (10 microM). However, in the ATP-depleted mesenteric artery (verified by high performance liquid chromatography), an increase in 86Rb+ efflux and a glibenclamide-induced enhancement of contraction were observed in the rat, but not in the dog. Taken together, between dog and rat mesenteric arterial strips, a differential effect of ATP depletion with 2-deoxyglucose plus oligomycin was identified buy micronase online in the activation of ATP-sensitive K+ channels, but not of cromakalim.

micronase drug interactions 2017-10-03

1. The aim of this study was to investigate whether the hypotensive effect of rat alpha-calcitonin gene-related peptide (alpha CGRP) in conscious rats is mediated by endothelium-derived nitric oxide (NO) or the opening of adenosine 5'-triphosphate (ATP)-sensitive potassium (KATP) channels. 2. Dose-mean arterial pressure (MAP)-response curves of alpha CGRP were examined in the presence of vehicle, phenylephrine, KATP channel antagonist glibenclamide or NO synthase inhibitors, NG-nitro-L-arginine methyl ester (L-NAME) and NG-nitro-D-arginine methyl ester (D-NAME). Dose-MAP-response curves for sodium nitroprusside were also constructed in buy micronase online the presence and absence of L-NAME and D-NAME. 3. alpha CGRP and nitroprusside produced dose-dependent reductions in MAP which were potentiated by phenylephrine. Both L-NAME and D-NAME attenuated the depressor response to alpha CGRP but not nitroprusside. 4. Dose-MAP-response curves for pinacidil, a KATP-channel activator, were also examined in the presence of glibenclamide or vehicle. Glibenclamide attenuated pinacidil- but not alpha CGRP-induced reductions in MAP. 5. It is concluded that the hypotensive effects of alpha CGRP are partially mediated via endothelium-derived NO but not via the opening of KATP channels.

micronase medication 2017-02-16

The critical time for opening mitochondrial (mito) K(ATP) channels, putative end effectors of ischemic preconditioning (PC), was examined. In isolated rabbit hearts 29+/-3% of risk zone infarcted after 30 minutes of regional ischemia. Ischemic PC or 5-minute exposure to 10 micromol/L diazoxide, a mito K(ATP) channel opener, reduced infarction to 3+/-1% and 8+/-1%, respectively. The mito K(ATP) channel closer 5-hydroxydecanoate (200 micromol/L), bracketing either 5-minute PC ischemia or diazoxide infusion, blocked protection (24+/-3 and 28+/-6% infarction, respectively). However, 5-hydroxydecanoate starting 5 minutes before long ischemia did not affect protection. Glibenclamide (5 micromol/L), another K(ATP) channel closer, blocked the protection by PC only when administered early. These data suggest that K(ATP) channel opening triggers protection but is not the final step. Five minutes of diazoxide followed by a 30-minute washout still reduced infarct size (8+/-3%), implying memory as seen with other PC triggers. The protection by diazoxide was not blocked by 5 micromol buy micronase online /L chelerythrine, a protein kinase C antagonist, given either to bracket diazoxide infusion or just before the index ischemia. Bracketing preischemic exposure to diazoxide with 50 micromol/L genistein, a tyrosine kinase antagonist, did not affect infarction, but genistein blocked the protection by diazoxide when administered shortly before the index ischemia. Thus, although it is not protein kinase C-dependent, the protection by diazoxide involves tyrosine kinase. Bracketing diazoxide perfusion with N:-(2-mercaptopropionyl) glycine (300 micromol/L) or Mn(III)tetrakis(4-benzoic acid) porphyrin chloride (7 micromol/L), each of which is a free radical scavenger, blocked protection, indicating that diazoxide triggers protection through free radicals. Therefore, mito K(ATP) channels are not the end effectors of protection, but rather their opening before ischemia generates free radicals that trigger entrance into a preconditioned state and activation of kinases.

micronase drug form 2015-12-04

In normo- or hyperglycemic (i.v. infusion of 50 mg/kg/min glucose over 30 min) pithed rats, diazoxide (1 mg/kg/min i.v. over 20 min) significantly reduced plasma insulin content. By contrast, cromakalim, nicorandil or RP 52891 even at doses 40-fold higher than those producing the same hypotensive effect as diazoxide in intact anesthetized normotensive rats, failed to change insulin plasma levels. Glibenclamide (0.01-0.3 mg/kg i.v.) pretreatment antagonized dose-dependently the hypoinsulinemic activity of diazoxide with an i.v. ED50 value of 49 +/- 1 microgram/kg. In pithed rats, diazoxide increased markedly plasma renin activity. This effect was almost inhibited completely by 20 mg/kg i.v., but buy micronase online not at all by a 1-mg/kg i.v. dose of glibenclamide. In pentobarbital-anesthetized rats, diazoxide (0.5-2 mg/kg/min i.v. over 20 min) produced decreases in mean carotid artery blood pressure which were antagonized dose-dependently by glibenclamide (5-20 mg/kg i.v.). This sulfonylurea (20 mg/kg i.v.) also prevented the hypotensive effects of several i.v. administered K+ channel activators (cromakalim, RP 52891 and nicorandil) but not those of numerous hypotensive agents such as acetylcholine, adenosine, bradykinin, clonidine, histamine, salbutamol, dihydralazine, papaverine, platelet aggregating factor, nitroglycerin, nitroprusside, nitrendipine and diltiazem. Although glibenclamide lowered plasma glucose levels, its blocking activity vis-à-vis the hypotension evoked by cromakalim was not affected when its hypoglycemic effects were reversed with an i.v. injection of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)

micronase dosing 2017-06-23

To determine the effects of pioglitazone in combination with buy micronase online sulphonylurea and metformin on diabetes control in patients being treated with insulin due to secondary failure of oral hypoglycemic agents.

micronase brand name 2017-02-19

Levosimendan, a compound that exerts effects on calcium sensitivity and intracellular free calcium, in addition to opening ATP-sensitive K-channels, is widely used in the treatment of buy micronase online heart failure. Because of its dual mechanism of action, we hypothesized that it would modulate human uterine contractility.

micronase buy cheap 2016-08-27

Short-circuit current (I(SC)) recording was used to measure epithelial ion transport. A scanning ion-selective electrode buy micronase online technique was used to directly measure Cl(-) flux (J(Cl)-) across the epithelium. RIA was used to measure emodin-induced histamine release.

micronase drug class 2017-07-26

Of the 175 products evaluated, 134 (77%) were found to be adulterated with Western drugs or their analogues. Most of these 134 samples (123 [92%]) were found to be adulterated with sildenafil. The extent of adulteration of these illegal health products with Western drugs, including synthetic phosphodiesterase type 5 enzyme (PDE-5) inhibitors, and the risks of consuming such illegal sexual enhancement products are discussed in this study. Because of the scope of the raids, sildenafil was the buy micronase online most common adulterant found. In addition, some products were found to contain high contents of sildenafil (>100 mg) and high contents of the antidiabetic drug, glibenclamide (glyburide). The resultant severe hypoglycaemia has led to ten fatalities.

micronase dosage 2017-05-09

Simultaneously administered magnesium hydroxide or sodium bicarbonate can increase the rate and extent of absorption of non-micronized glibenclamide and glipizide. To clarify the mechanism of this interaction we have studied the effect of pH on the dissolution of two different formulations of glibenclamide (micronized and non-micronized) and one formulation of glipizide. One tablet of each sulphonylurea preparation was placed in a dissolution chamber containing continuously mixed dissolution medium at pH 2, pH 6 or pH 9; 5 mL of the medium was replaced every 2 min. The amount of glibenclamide dissolved from the non-micronized formulation within 2 h, was 1.2, 4.5 and 76% at pH buy micronase online 2, pH 6 and pH 9, respectively (P < 0.01), whereas 21, 29 and 100% was dissolved from the micronized formulation (P < 0.01). The amount of glipizide dissolved within 2 h at pH 2, pH 6 and pH 9 was 3.9, 24 and 92%, respectively (P < 0.01). We conclude that the elevated pH of the gastric contents is the most likely explanation for the interactions previously demonstrated between antacids and sulphonylureas after their concomitant ingestion.

micronase 50 mg 2017-09-12

Phyllanthus amarus has been used in traditional medicine in Nigeria to treat some disease conditions. This study evaluated the soft drink extract (SDE) of buy micronase online the plant for antidiabetic activities in rats.

micronase tablets 2015-11-11

Hypoxia (O(2) tension approximately 20 mmHg) dilated endothelium-denuded porcine coronary arterial rings precontracted with Zantac Overdose Infant high K(+) in the presence of glibenclamide (5 microM), a blocker of K(ATP) channels. In dispersed human and porcine myocytes, low O(2) tension decreased basal cytosolic [Ca(2+)] and transmembrane Ca(2+) influx independently of K(+) channel activation. In patch clamped cells, hypoxia reversibly inhibited L-type Ca(2+) channels. RT-PCR indicated that rHT is the predominant mRNA variant of the alpha(1C) Ca(2+) channel subunit in human coronary myocytes.

micronase generic name 2017-09-19

Glyburide (glibenclamide) is a sulfonylurea derivative that is very widely used in the treatment of type II diabetes mellitus. Currently, there are several pharmaceutical formulations available in Mexico containing this drug, however, very limited information about their bioavailabilities is known. The purpose of this study was to compare the bioavailability of two formulations of glyburide used in Mexico, Daonil and Gen-Glybe. Twenty-four Mexican healthy volunteers participated in this study that was carried out following the recommendations of the Declaration of Helsinki. Subjects received a dose of 10 mg of glyburide (two tablets of 5 mg) under fasting conditions in two separate sessions using a randomized crossover design with a one week washout period. Plasma samples were obtained at selected times over 24 hours and stored frozen until analyzed. Pharmacokinetic parameters were obtained and values (mean +/- S.E.M.) were as follows: Cmax 273.32 +/- 25.84 versus 294.83 +/- 27.12 ng/ml; tmax 3.03 +/- 0.23 versus 2.87 +/- 0.24 h; and AUC24h 1396.66 +/- 130.18 versus 1557.99 +/- 140.24 ng x h/ml, for Daonil and Gen-Glybe tablets, respectively. Pharmacokinetic parameters were compared using analysis of variance for a cross-over design and ratios of AUC24h and Cmax and 90% confidence intervals were obtained. As Calan 180 Mg confidence intervals did not exceed the limits of acceptance (80--125%) for Cmax and AUC24h, it is concluded that the formulations tested are bioequivalent.

micronase drug information 2017-08-25

The sulphonylureas glibenclamide and tolbutamide inhibited carnitine acyltransferase activities in rat liver microsomes. Glibenclamide was a more potent inhibitor than tolbutamide. The effect of tolbutamide on the malonyl-CoA-inhibitable transferase was influenced by the phospholipid/detergent environment whereas the effect of Artane 4 Mg glibenclamide was not. Glibenclamide was a more potent inhibitor of the malonyl-CoA-inhibitable transferase than of the malonyl-CoA-insensitive enzyme. The extent of inhibition of the malonyl-CoA-inhibitable transferase by tolbutamide was similar to its effect on VLDL triacylglycerol secretion as reported by Wiggins and Gibbons [Biochem. J. 284 (1992) 457-462] possibly supporting the suggestion that microsomal carnitine acyltransferases are involved in VLDL triacylglycerol assembly/secretion.

micronase 10 mg 2017-02-16

Investigation of combination therapy with tamoxifen and K+ Depakote 7 Mg channel-blockers is warranted.

micronase cost 2016-09-26

To analyze the mechanism of action of adrenomedullin (AM), a peptide recently isolated from human pheochromocytoma Cardura 40 Mg , in isolated canine central retinal arteries and to compare the action of calcitonin gene-related peptide (CCRP).

micronase 5 mg 2016-02-17

Troglitazone, a newly developed thiazolidinedione derivative, has been shown to ameliorate microalbuminuria in diabetic animal model and in human diabetic nephropathy in short-term studies. The aim of the present study was to determine whether troglitazone or sulphonylurea affect micro- albuminuria Order Viagra Australia , macroalbuminuria, or serum type IV collagen concentrations in patients with diabetic nephropathy.

dosage of micronase 2016-11-27

The occurrence and severity of hypoglycaemic symptoms were associated with increased patient worry about hypoglycaemia and lower health-related quality of life among type 2 diabetic patients being treated with Singulair 5mg Tablets both metformin and a sulphonylurea.

micronase drug interactions 2015-04-06

Ketamine, but not S(+)-ketamine blocks the cardioprotective effect of ischemic Ondansetron Zofran Dosage preconditioning in vivo.

micronase medication 2016-05-11

NOD-like receptors (NLRs) sense sterile and non-sterile signals and form inflammasomes which trigger an inflammatory response through the activation of caspase-1 and release of IL-1β. Recently we have shown the presence of several NLRs in the bladder urothelia and demonstrated the importance of NLRP3 in bladder outlet obstruction and cyclophosphamide-induced Generic Cymbalta Release cystitis, both models of sterile inflammation. In this study we explore a role for NLRP3 in mediating the response to LPS, a key antigen of uropathogenic bacteria.

micronase drug form 2015-11-20

Serum concentrations and blood glucose lowering effects (expressed as percent blood glucose reduction vs placebo) of glibenclamide (Gb) and its active metabolites, 4-trans-hydroxy-(M1) Ventolin Tablets and 3-cis-hydroxy-glibenclamide (M2), were analysed in eight healthy subjects participating in a placebo-controlled, randomized, single-blind crossover study, using intravenous administration of each compound as well as oral administration of Gb.

micronase dosing 2016-05-13

An acute increase in insulin levels in Lopressor Drug Classification portal blood peaked at 15 min in the NAT group, while insulin levels in the GB group continued to increase significantly after 60 min. Glucose levels in peripheral blood were significantly lower in the NAT group at 30 and 60 min and in the GB group at 120, 180 and 270 min after glucose loading, compared with those in the vehicle group. Subsequently, fasting rats were given NAT, GB or vehicle and then immediately given oral fat emulsion (soy oil 2 g/kg). An acute increase in insulin secretion was seen with NAT, peaking at 30 min, while TG, chylomicron and very low-density lipoprotein levels after fat loading were shown to be significantly lower with NAT than with vehicle. However, the continued insulin secretion observed with GB led to no significant decrease in TG levels after fat loading. In addition, lipoprotein lipase mRNA expression in adipose tissue increased significantly 120 min after NAT administration in comparison with baseline. This increase was not noted with GB administration.

micronase brand name 2016-08-27

1. Openers of the ATP-sensitive potassium channel (KATP channel) increase and blockers decrease renin secretion. Here we report the effects of levcromakalim (LCRK, a channel opener) and glibenclamide (GBC, a blocker) on membrane potential, whole-cell current and the cytoplasmic Ca2+ concentration of renin-secreting cells (RSC). Studies were performed on afferent arterioles from the kidney of Na+-depleted rats. 2. As monitored with the fluorescent oxonol dye DiBAC4(3), LCRK (0.3 and 1 microM) induced a hyperpolarization of approximately 15 mV which was abolished by GBC (1 microM). 3. Whole-cell current-clamp experiments showed that RSC had a membrane potential of -61 +/- 1 mV (n = 16). LCRK (1 microM) induced a hyperpolarization of 9.9 +/- 0.2 mV (n = 16) which, in the majority of cells, decreased slowly with time. 4. Capacitance measurements showed a strong electrical coupling of the cells in the preparation. 5. At -60 mV, LCRK induced a hyperpolarizing current in a concentration-dependent manner with an EC50 of 152 +/- 31 nM and a maximum current of about 200 pA. 6. Application of GBC (1 microM) produced no effect; however, when applied after LCRK (300 nM), GBC inhibited the opener-induced hyperpolarizing current with an IC50 of 103 +/- 36 nM. 7. LCRK (0.3 and 1 microM) did not significantly affect the cytoplasmic Ca2+ concentration either at rest or after stimulation by angiotensin II. 8. The data show that LCRK induces a GBC-sensitive hyperpolarizing current in rat RSC. This current presumably originates from the activation of KATP channels which pharmacologically resemble those in vascular smooth muscle cells. The stimulatory effect of KATP channel opening on renin secretion is not mediated by a decrease in intracellular Ca2+ concentration.

micronase buy cheap 2017-09-30

At week 20, patients taking glyburide/metformin 1.25/250 mg or 2.5/500 mg tablets had greater reductions in HbA1c levels (-1.48% and -1.53% respectively) compared with placebo (-0.21%; both p < 0.001), glyburide (-1.24%; p = 0.016 and p = 0.004 respectively) or metformin (-1.03%; both p < 0.001). Fasting plasma glucose concentrations were reduced more in both glyburide/metformin groups compared with placebo and metformin (p < 0.001); patients in both combination therapy groups also had significantly lower postprandial glucose concentrations compared with placebo, glyburide and metformin.

micronase drug class 2017-09-14

It has been reported that hydrogen sulfide (H(2)S) could relax vascular smooth muscle by direct activation of K(ATP) channels and hyperpolarization of the membrane potential. Recently, our study has shown that H(2)S facilitated carotid baroreflex. This study was conducted to investigate the effect of H(2)S on carotid baroreceptor activity (CBA).

micronase dosage 2016-10-27

We studied eight women who had received a single oral dose of 5 or 10 mg glyburide. Drug concentrations were measured in maternal blood and milk for 8 h after the dose. In a separate study, five women were given a daily dosage (5 mg/day) of glyburide or glipizide, starting on the first postpartum day. Maternal blood and milk drug concentrations and infant blood glucose were measured 5-16 days after delivery.

micronase 50 mg 2015-04-16

Endothelin-1 (ET-1) is a polypeptide that has potent hemodynamic effects on the pulmonary circulation. To determine whether there are changes in these effects with increasing postnatal age, we investigated the effects of ET-1 (250 ng/kg) at rest and during pulmonary hypertension in eight lambs (< 1 wk old) and 11 juvenile sheep (6-12 mo old). At rest, ET-1 did not change pulmonary arterial pressure in lambs, but increased pulmonary arterial pressure by 64.0 +/- 37.5% (p < 0.05) in sheep. During pulmonary hypertension, ET-1 produced greater decreases in pulmonary arterial pressure in lambs than in sheep (26.6 +/- 3.4% versus 18.7 +/- 8.3%, p < 0.05). In juvenile sheep, the increase in resting pulmonary arterial pressure produced by ET-1 was inhibited by meclofenamic acid, an inhibitor of prostaglandin synthesis (40.3 +/- 9.9% versus 2.3 +/- 4.7%, p < 0.05); during pulmonary hypertension, the decrease in pulmonary arterial pressure produced by ET-1 was inhibited by N omega-nitro-L-arginine, an inhibitor of endothelium-derived nitric oxide synthesis (21.4 +/- 10.7% versus 8.0 +/- 3.6%, p < 0.05) and by glybenclamide, an ATP-dependent potassium-channel blocker (18.8 +/- 8.4% versus 4.0 +/- 4.4%, p < 0.05). The hemodynamic effects of ET-1 on the pulmonary circulation are dependent on postnatal age. Pulmonary vasoconstriction is mediated by prostaglandin production, and pulmonary vasodilation is mediated, in part, by release of endothelium-derived nitric oxide and activation of ATP-dependent potassium channels.