Nifedipine
Adrenergic receptor pathways. Using primary neonatal rat cardiac myocytes, we showed that NE markedly stimulated the rat ET-1 promoter activity and that this stimulation was severely attenuated by the -adrenergic receptor blocker metoprolol but not by the -adrenergic receptor blocker prazosin. In addition, ET-1 promoter activity was activated by the -adrenergic agonist ISO to an extent similar to the activation by NE. These findings indicate that NE-inducible expression of ET-1 in cardiac myocytes is controlled, at least in part, at the level of transcription and that NE stimulation of ET-1 transcription is mediated predominantly via a -adrenergic pathway. -adrenergic stimulation results in an increase in the intracellular calcium level. The present study demonstrated that -adrenergic agonist-stimulated ET-1 transcription was significantly inhibited by the calcium antagonist nifedipine. This finding suggests that calcium signaling may be involved in this proc. In 9193 participants aged 55-80 years with essential hypertension in blood pressure lowering between the angiotensin receptor blocker losartan and atenolol, however, a 25% reduction of the relative risk of stroke was observed in the losartan group during the follow-up period of 4.8 years. The results of this study may imply that the angiotensin receptor blocker losartan could confer benefits beyond the blood pressure reduction9. The Study on Cognition and Prognosis in the Elderly SCOPE ; randomized 4964 elderly patients with mild to moderate hypertension to the angiotensin receptor blocker candesartan or placebo, and followed them up for 4.5 years. The candesartan group showed a 10.9% reduction in the relative risk of stroke, myocardial infarction or death. The candesartan-based treatment reduced nonfatal stroke by 27.8% and all stroke by 23.6%. The large reduction of nonfatal and all stroke could implicate that the angiotensin receptor blocker candesartan could have some additional effects in stroke prevention besides blood pressure lowering10. On the other hand, calcium antagonists, especially the highly lipophilic ones, amlodipine nad lacidipine, may have some antioxidant properties. These drugs reduce the oxidation of LDL cholesterol and its influx into the arterial wall, and reduce atherosclerotic lesions in animals. Platelet production is suppressed by amlodipine, lacidipine or nifedipine in hypertensive patients. Thus, selective calcium antagonists could be potential antiatherosclerotic agents11. New evidence from longterm clinical trials of calcium antagonists indicate that these drugs can reduce the rate of atherosclerosis progression in hypertensive and coronary heart disease patients. In the Regression Growth Evaluation Statin Study REGRESS ; , coadministration of the calcium antagonist amlodipine or nifedipine with pravastatin caused a significant reduction in the occurrence of new angiographic lesions12, 13. In the Verapamil in Hypertension and Atherosclerosis Study VHAS ; , verapamil was more effective than chlorthalidone in promoting regression of thicker carotid lesions in parallel with a reduction in the incidence of cardiovascular events14. In the Prospective Randomized Evaluation of the Vascular Effects of Norvasc Trial PREVENT ; , amlodipine slowed the progression of early coronary atherosclerosis in patients with coronary artery disease6. In a subprotocol of the Interventions as a Goal in the Hypertension Treatment INSIGHT ; study, nifedipine gastrointestinal-transport-system GITS ; significantly decreased intima media thickness as compared with coamilozide hydrochlorothiazide + amiloride ; 15!
Releasing intracellular Ca 2 + phospholipase C-independent manner and by causing nifedipinesensitive Ca 2 + influx. Key Word: Ca 2 + signaling, clomiphene, fura-2, MG63 cells, osteoblasts. 43 effect of nifedipine, captopril and prazosin on secretory function of pancreatic beta-cells in hypertensive patients with type-2 non-insulin-dependent ; diabetes and in hypertensive non-diabetics. FIG. 3. Scatchard analysis of ionic interactions. Saturation binding experiments were carried out on EGTA-washed membranes in the absence of ions i ; or in the presence of 1 mM CaCl2 0.1 mM LaCl3 A ; , 1 mM CaCl2 0.03 mM LaCl3 A ; , 1 mM CaCl2 1 mM CoC12 0 ; , or 1 CaCl2 alone A ; . Total and nonspecific [3H]nitrendipine binding were determined in triplicate at nine concentrations of [3H]nitrendipine between 0.005 and 2.0 nM in the absence and presence of 60 nM nifedipine, respectively. Data presented are from a representative experiment that was replicated two or three times with similar results.
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Hormonal medications, such as contraceptives and hormone replacement therapy, also may worsen migraines. Pseudoaddiction Drug seeking behaviors that occur when pain is undertreated and mimic addictive behaviors. Diversion The misappropriation of opioids for a user other than the person for whom they were prescribed. Diversion is often motivated by monetary gain and selegiline, for example, nifedipine 30mg. Rx Only 2004 B. Braun Medical Inc. All Rights Reserved. Y07-530-356-1 04 DUPLEX is a registered trademark of B. Braun Medical Inc. The P and T committee decided to take it off about two weeks ago but unfortunately we haven't gotten the memo out yet. Oh wow. The formulary around here changes so darn often. Yeah. Frankly, it's confusing for us, too. The major issue is cost. Amlodipine is much more expensive than generic diltiazem or generic nifedipine. I understand that, but my patient didn't tolerate either of those because of edema, and I've read that amlodipine tends to cause less edema than either nifedipine or diltiazem. That's true. Can I suggest a few other options? Sure. Go ahead. You could leave the patient on diltiazem and add a diuretic for the edema. I'd prefer not to use a diuretic because he also has gout and hyperlipidemia and sinemet. Drugs may have a profound effect on lower urinarytract function, although there are no drugs that have specific effects on the bladder and urethra and do not affect other tissues or organs. Drugs can change the autonomic function of the bladder by affecting the cholinergic and adrenergic nerves. There are also many co-transmitters and local hormones that act on the lower urinary tract including histamine, 5-hydroxytryptamine, substance P, endogenous opioids, vasoactive intestinal peptide, neuropeptide Y and prostaglandins. The importance of these substances in the normal function of the bladder and urethra is not clear but their effects can be blocked by anticholinergics and adrenergic blockers. There are many drugs available to treat an overactive detrusor: Anticholinergic drugs: propantheline bromide emepronium bromide carrageenate Musculotrophic drugs: oxybutynin chloride dicyclomine chloride flavoxate hydrochloride Calcium antagonists: nifedipine flunarizine Tricyclic antidepressants: imipramine doxepin Beta ; -adrenoceptor agonists: terbutaline salbutamol isoprenaline Alpha ; -adrenoceptor antagonists: phenoxybenzamine prazosin.
Table III. Up-regulation of genes in the endometria of patients with endometriosis compared to normal endometria of the secretory phase GenBank accession number U62015 M92843 D90097 L13740 X53587 J05428 X68277 M92934 L11329 U20734 U82319 U48296 X52541 V01512 X62048 X51345 S78825 U59914 AF010193 L13720 M27281 X01703 Gene description Secretory phase: 20 comparisons up down ; 18 0 16 Average fold change 5.0 4.0 2.7 and hytrin.
And diphenylpiperazine flunarizine, both blockers of T-type Ca channels Wang et al. 1990 ; . As shown in Fig. 2D the voltage-activated current was blocked by both agents. Consistent with this behaviour was the finding that nifedipine and -conotoxin blockers of L-type and N-type Ca channels, respectively ; had no effect data not shown ; . Since both L and N-type Ca channels are activated at high voltages, we confirmed the absence of these channels by adding NiCl or flunarizine. As expected, stimulation of cells to more depolarized potentials from a holding potential of -60 mV did not elicit inward currents. Taken together, these findings indicated that SK-N-MC cells express the low voltage-activated T-type ; Ca channels but not the high voltage-activated ones.
In the recent study on a new variant of the cytochrome P450 3A4 CYP3A4 ; gene by Rebbeck et al. 1 ; , the authors did not provide data that demonstrate an alteration of CYP3A4 function as a consequence of the polymorphism. They suggested that the variant allele might alter disposition of the androgenic substrates of CYP3A4 as a result of decreased enzymatic activity. Worse clinical presentation of prostate cancer 1 ; and a decreased risk for treatment-related leukemia 2 ; were reported to be associated with the variant allele, the former probably due to increased bioavailability of testosterone and the latter probably due to reduced production of leukemogenic metabolites of anticancer drugs. Thus, we investigated the possible relationship between CYP3A4 genotypes and nifedipine oxidation activity, a prototype reaction of the encoded enzyme, by use of a human liver microsome system in vitro. Fifteen liver samples from Caucasian transplant donors were obtained from the National Disease Research Interchange Philadelphia, PA ; through the Biomedical Research Institute, Human and Animal Bridge Discussion Group Chiba, Japan ; . The nifedipine oxidation activity and the expression levels of CYP3A4 protein of the samples have been reported elsewhere 3 ; . A variant sequence of the CYP3A4 gene was distinguished from wild-type by a nested polymerase chain reactionrestriction fragment length polymorphism assay by the use of genomic DNA prepared from the liver samples Fig. 1, A ; . The institutional review board of St. Marianna University School of Medicine has approved the study. The genotyping analysis revealed one homozygote and four heterozygotes for the variant. The remaining 10 subjects were homozygous for the wild-type allele. No apparent relationships between the genotypes and the activity or amount of CYP3A4 were found Fig. 1, B ; . Moreover, we examined the distribution of the new polymorphism in the Japanese population. DNA samples were prepared from 128 unrelated and aripiprazole!
The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure JNC VI ; . Arch Intern Med 1997; 157: 2413-45. Fuchs FD, Lubianca Neto JF, Neves JM - Urgncia e emergncia hipertensivas. Arq Bras Cardiol 1991; 56: 243-6. Ellrodt AG, Ault MJ, Riedinger MS, Murata GH - Efficacy and safety of sublingual nifedipine in hypertensive emergencies. J Med 1985; 79 suppl 4A ; : 19-25. Grossman E, Messerli FH, Grodzicki T, Kowey P - Should a moratorium be placed on sublingual nifedipine capsules given for hypertensive emergencies and pseudoemergencies? JAMA 1996; 276: 1328-31. Andrighetto AG, Pilla MB, Kronbauer AL, et al - Prevalncia de consultas em. This study examined direct effects of these drugs on ache activity in the frontal, temporal, and parietal cortices in ad and quinapril.
Let's see the types of treatment by bacterial vaginosis medicines: conventional bacterial vaginosis treatment: bacterial vaginosis is most effectively treated by antibiotics, for instance, nifedipine sustained release. Many natural products and bioactive agents such as nifedipine, 1 nitrendipine2 and felodipine3 are 1, 4-dihydropyridine derivatives 1, 4-DHPs ; . The coenzyme reduced nicotinamide adenine dinucleotide NADH ; is the cofactor used by many reductases in metabolism, and its reactive moiety is a 1, 4-DHP unit. Compounds based on this heterocycle play key roles in therapeutic and bioorganic chemistry4 for treatment of a variety of diseases, such as cardiovascular disorders, 4a cancer4b and AIDS.4c Recent papers have reported novel 1, 4-DHP derivatives as calcium channel modulators, 5 as Ca-blockers against endothelial cell oxidative injury, 6 with vasodilating activity7 and as nonpeptide HIV-1 protease inhibitors.8 On the other hand, 1, 4-DHPs are also used as versatile intermediates in organic synthesis.9 Several groups have prepared diversely substituted 1, 4-DHP derivatives, however, potential applications in the aforementioned fields remain elusive or unknown. Reduction of Nalkylpyridinium salts10 or regioselective addition of nucleophilic reagents to N-acylpyridinium ions11 are the most simple and reliable methods for the regioselective formation of the corresponding 1, 4-DHP derivatives. Furthermore, few examples of 2, 6-disubstituted and aceon.
Clive Holmes is Senior Lecturer in Old Age Psychiatry in the Faculty of Medicine, Health and Biological Sciences at the University of Southampton Thornhill Research Centre, Moorgreen Hospital, Botley Road, West End, Southampton SO30 3JB; tel 01703 475216; fax 01703 463022 ; and Honorary Consultant old age psychiatrist at the Western Community Hospital in Southampton. David Wilkinson is a consultant in old age psychiatry and Honorary Senior Lecturer based in Southampton. He established the Thornhill Research Unit in 1990, which has been involved in over 30 multi-centre and international phase II and phase III trials.
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Everyone complains about diabetes and weight gain; here's a drug that likely doesn't have these problems.
2005; 293 8 ; : 935-94 melville jl, newton k, fan my, katon health care discussions and treatment for urinary incontinence in women and sumycin and nifedipine, for instance, nifedipinee extended release tablets.
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NIFEDIPINE Sigma Prod. No. N7634!
Several investigators report that calcium channel blockers, particularly nifedipine, relieves pain associated with many cases of piloleiomyomas. Clinical Studies: ADALAT CC produced dose-related decreases in systolic and diastolic blood pressure as demonstrated in two double-blind, randomized, placebo-controlled trials in which over 350 patients were treated with ADALAT CC 30, 60 or 90 mg once daily for 6 weeks. In the first study, ADALAT CC was given as monotherapy and in the second study, ADALAT CC was added to a beta-blocker in patients not controlled on a beta-blocker alone. The mean trough 24 hours post-dose ; blood pressure results from these studies are shown below: MEAN REDUCTIONS IN TROUGH SUPINE BLOOD PRESSURE mmHg ; SYSTOLIC DIASTOLIC STUDY 1 ADALAT CC N MEAN TROUGH DOSE REDUCTION * 30 MG 60 5.3 2.9 MG 57 8.0 4.1 MG 55 12.5 8.1 STUDY 2 N MEAN TROUGH ADALAT CC DOSE REDUCTION * 30 MG 58 7.6 3.8 MG 63 10.1 5.3 MG 62 10.2 5.8 * Placebo response subtracted. The trough peak ratios estimated from 24 hour blood pressure monitoring ranged from 41%-78% for diastolic and 46%-91% for systolic blood pressure. Hemodynamics: Like other slow-channel blockers, nifedipihe exerts a negative inotropic effect on isolated myocardial tissue. This is rarely, if ever, seen in intact animals or man, probably because of reflex responses to its vasodilating effects. In man, nifedipine decreases peripheral vascular resistance which leads to a fall in systolic and diastolic pressures, usually minimal in normotensive volunteers less than 5-10 mm Hg systolic ; , but sometimes larger. With ADALAT CC, these decreases in blood pressure are not accompanied by any significant change in heart rate. Hemodynamic studies of the immediate release nifedipine formulation in patients with normal ventricular function have generally found a small increase in cardiac index without major effects on ejection fraction, left ventricular end-diastolic pressure LVEDP ; or volume LVEDV ; . In patients with impaired ventricular function, most acute studies have shown some increase in ejection fraction and reduction in left ventricular filling pressure. Electrophysiologic Effects: Although, like other members of its class, nifedipine causes a slight depression of sinoatrial node function and atrioventricular conduction in isolated myocardial preparations, such effects have not been seen in studies in intact animals or in man. In formal electrophysiologic studies, predominantly in patients with normal conduction systems, nifedipine administered as the immediate release capsule has had no tendency to prolong atrioventricular conduction or sinus node recovery time, or to slow sinus rate. INDICATION AND USAGE ADALAT CC is indicated for the treatment of hypertension. It may be used alone or in combination with other antihypertensive agents. CONTRAINDICATIONS Known hypersensitivity to nifedipine.
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