Drugs online research references
Pharmacol Res. 1998 Oct;38(4):317-22.
L-type calcium channels modulate the regression of left ventricular hypertrophy after ace-inhibition in genetic hypertension.
Vulpis V, Lograno MD, Seccia TM, Pirrelli A.
Department of Internal Medicine, DIMO, Piazza G. Cesare, 11, Bari, 70124, Italy.
The aim of this study was to investigate the possible link between the regression of the left ventricular mass induced by ACE-inhibition and L-type calcium channels. For this purpose, an evaluation of both L-type calcium channels and AT1 receptor patterns in the left ventricular tissue of adult spontaneously hypertensive rats (SHR) was made before and after long-term treatment with ramipril. An abnormal density of both dihydropyridine and AT1 receptors was observed in SHR at 24 weeks, compared to age-matched control Wistar-Kyoto (WKY) rats (dihydropyridine receptor Bmax: 1. 30+/-0.09 vs 1.14+/-0.06 pmol mg-1 proteins, P<0.001; AT1 receptor Bmax: 1.35+/-0.07 vs 2.62+/-0.08, P<0.001 pmol mg-1 proteins). A treatment for 10 weeks with ramipril induced a significant decrease in the left ventricular mass index of SHR, as well as a significant decrease in dihydropyridine receptor density (Bmax: 0.96+/-0.01 vs 1. 39+/-0.08 pmol mg-1 proteins, P<0.001) and a significant increase in AT1 receptor density (Bmax: 3.08+/-0.26 vs 2.78+/-0.09 pmol mg-1 proteins, ramipril-treated SHR vs vehicle-treated SHR, P<0.001). These results suggest that the decrease in left ventricular mass after treatment with ramipril may be dependent on changes in L-type calcium channels other than the direct effect on circulating and tissue angiotensin II (ang II) levels: involvement of calcium channels and subsequent calcium influx into cardiac cells could be proposed as an additional mechanism for the regression of left ventricular mass after ACE-inhibition. Copyright 1998 The Italian Pharmacological Society
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9774496&dopt=Abstract
Hypertension. 1994 Aug;24(2):157-62.
Interrelation between renin mRNA levels, renin secretion, and blood pressure in two-kidney, one clip rats.
Schricker K, Holmer S, Hamann M, Riegger G, Kurtz A.
Physiologisches Institut, Universitat Regensburg, Germany.
To examine the interrelation between renin mRNA levels, renin secretion, and blood pressure in rats, we clipped the left renal arteries of rats and measured renin mRNA levels in both kidneys, plasma renin activity, and blood pressure. One and 2 days after clipping, renin mRNA levels increased 3-fold and 4.3-fold in the stenosed kidney and were suppressed to 52% and 26% of controls in the intact kidneys; plasma renin activity increased from 8 to 16.5 and to 30.5 ng angiotensin I.h-1.mL-1 and systolic blood pressure rose from 114 to 123 and to 137 mm Hg. We found a strong correlation (P < .001) between plasma renin activity and renin mRNA levels in the clipped kidneys. We also found significant correlations (P < .05) between mRNA levels in the clipped and intact kidneys and between plasma renin activity and blood pressure for the individual animals. Treatment of normal rats with the converting enzyme inhibitor ramipril (5 mg/kg twice a day) for 2 days increased renin mRNA levels in both kidneys fourfold. In animals with unilateral clips, additional treatment with ramipril increased renin mRNA levels 6.4-fold in the stenosed and 3.3-fold in the intact kidneys. These findings suggest that endogenous angiotensin II exerts an inhibitory effect on renin mRNA expression in normal kidneys, clipped kidneys, and their contralaterals. Suppression of the renin gene in contralateral kidneys seems not to be directly mediated by the rise of plasma renin activity or by the rise of blood pressure in two-kidney, one clip rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8039838&dopt=Abstract
Clin Exp Pharmacol Physiol Suppl. 1995 Dec;22(1):S347-9.
Effect of angiotensin-converting enzyme inhibitors on fructose induced hypertension and hyperinsulinaemia in rats.
Erlich Y, Rosenthal T.
Chorley Institute of Hypertension, Chaim Sheba Medical Center, Tel Hashomer, Israel.
1. The effect of angiotensin-converting enzyme inhibitors (ACEI) enalapril, lisinopril and ramipril was studied on fructose-induced hypertensive and hyperinsulinaemic rats. 2. 60 Sprague-Dawley rats were fed a fructose-enriched diet for 5 weeks, which produced hyperinsulinaemia, hypertriglyceridaemia and hypertension. Beginning with week 3 of the diet, lisinopril (10 and 20 mg per kg per day), ramipril (5 and 10 mg/kg per day) and enalapril (20 mg/kg per day) were given daily in drinking water for 2 weeks to 10 rats in each drug group. Ten rats fed only the fructose-enriched diet served as control. 3. Systolic blood pressure was measured weekly by the indirect tail-cuff method. Plasma insulin level was determined using RIA. 4. Data indicate that ACEI improve insulin resistance induced by high-fructose intake in rats; that despite their equal hypotensive effect, ACEI differ in their ability to improve insulin resistance; and that improvement of insulin resistance by ACEI is dose-dependent.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9072423&dopt=Abstract
Herbs and Pharmaceuticals Online ||
Hair Million herbal formula for hair loss and hair growth ||
Wellstreet online pharmacy for click-order prescription medications ||
Altace Online Pharmacy ||
Rx Drugs USA, Prescription Drugs Online Pharmacy ||
Insurance plans and information ||
Insurance policies for all purposes ||
Antibiotics and prescription medications online literature ||