Drugs online research references
J Pharm Pharmacol. 1988 Jul;40(7):514-5.
Verapamil and nifedipine effects on gastric acid secretion and ulcer formation in rats.
Glavin GB.
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
The calcium channel antagonists verapamil and nifedipine were examined for their effects on conscious basal gastric acid output, stress ulcer formation and on ethanol-induced ulcers. Both compounds significantly reduced gastric acid secretion, however verapamil did so in a dose-related manner. Both verapamil and nifedipine significantly attenuated stress gastric ulcer formation. Nifedipine, at a dose of 32.0 mg kg-1, virtually abolished stress ulcers. Verapamil exacerbated, while nifedipine, at 32.0 mg kg-1, attenuated ethanol-induced gastric ulcers. The differential gastrointestinal effects of these calcium channel antagonists support the existence of multiple classes of calcium channels in the gut and suggest an important role for intracellular calcium and hence, its blockade, in gastric pathophysiology.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2904996&dopt=Abstract
Eur J Pharmacol. 1985 Jul 11;113(1):25-36.
Renal and cardiovascular effects of acute and chronic administration of felodipine to SHR.
Nordlander M, Di Bona GF, Ljung B, Yao T, Thoren P.
Renal function and salt and water turnover were studied in SHR during acute and chronic administration of felodipine, which is an efficient antihypertensive vasodilating Ca2+ antagonist. In conscious SHR acute administration of felodipine in hypotensive doses increased renal sympathetic nerve activity but caused renal vasodilation, increases in GFR and a 2-3 fold increase in urinary flow rate and sodium excretion. The fraction of filtered sodium excreted (FENa) was approximately doubled. The diuretic and natriuretic effects of felodipine are therefore suggested to be due to a direct inhibitory action on the renal tubular cells, resulting in reduced sodium reabsorption. Nifedipine also induced diuresis and natriuresis in this system, while minoxidil reduced water and sodium excretion. Throughout 6 months of felodipine treatment, the mean arterial pressure (MAP), remained 25-20 per cent reduced. Felodipine in combination with metoprolol reduced MAP 25-30 per cent and also caused regression of left ventricular hypertrophy, while felodipine alone prevented its further progression. Also during chronic administration, felodipine induced diuresis but had no effect on plasma volume and on sodium or potassium excretion in SHR. It is concluded that in SHR felodipine induces diuresis; on acute treatment this is secondary to reduced tubular sodium reabsorption, although during chronic treatment the sodium loss is compensated for while the diuresis remains. Thus, the cardiovascular and renal effects of Ca2+ antagonists like felodipine differ substantially from those of other potent antihypertensive vasodilators e.g. minoxidil.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2931282&dopt=Abstract
Acta Cardiol. 1987;42(1):37-47.
Slow-release nifedipine: effect on the circadian rhythm of blood pressure in essential hypertension.
Portaluppi F, degli Uberti E, Strozzi C, Margutti A, Montanari L, Rambaldi R, Trasforini G, Pansini R.
The aim of this study was to investigate the effect of orally administered, slow-release, nifedipine tablets on the circadian rhythm of blood pressure and heart rate, in hospital patients with clinical diagnosis of hypertension validated by a chronobiologic inferential statistic method. A group of 14 patients (nine women and five men, 47 to 71 years old) with clinical diagnosis of "essential hypertension" underwent automatic blood pressure and heart rate monitoring in a hospital room for 48 hours. Measurements were taken every 15 min by an oscillometric instrument with automatically inflated cuff. The patients received no treatment during the two proceeding weeks and the first day of the study. On the second day, slow-release nifedipine tablets were administered, one at 10 a.m. and one at 10 p.m. A highly significant circadian rhythm was documented for systolic and diastolic blood pressure, mean arterial pressure and heart rate, both in basal conditions and after nifedipine. Blood pressure mesors were higher than reference standards in basal conditions, and were lowered (average decrease = 20 mmHg for systolic and 9 mmHg for diastolic mesor) by nifedipine. A significant, though minor, elevation of heart rate mesor (from 70 to 75 b.p.m.) was also noted during treatment. The circadian amplitudes of blood pressure and heart rate did not differ significantly before and during treatment. In conclusion, the circadian rhythm of blood pressure is still present with the same amplitude after slow-release nifedipine, but is set at a lower pressure level. Heart rate rhythm is also preserved, with only a minor elevation of its mesor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3494367&dopt=Abstract
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