Drugs online research references
Hypertension. 1987 Feb;9(2):150-6.
Comparison of a new renin inhibitor and enalaprilat in renal hypertensive dogs.
Smith SG 3rd, Seymour AA, Mazack EK, Boger J, Blaine EH.
The hypotensive efficacy of a potent new renin inhibitor (N alpha-isovaleryl-L-histidyl-L-prolyl-L-phenylalanyl-L-histidyl-ACHPA+ ++-L- phenylalanyl amide) containing (3S,4S)-4-amino-5-cyclohexyl-3-hydroxy pentanoic acid (ACHPA) was compared with the converting enzyme inhibitor (enalaprilat) (MK-422) in conscious one-kidney dogs before and after tightening a renal artery clamp. Dose-response curves to 0.003 to 0.1 mg/kg/min i.v. infusions of the ACHPA-containing renin inhibitory peptide or enalaprilat (0.003-0.1 mg/kg i.v. bolus) were obtained in one-kidney dogs before and 3 days and 14 days after renal artery constriction. The ACHPA-containing renin inhibitory peptide and enalaprilat maximally decreased blood pressure by 10 +/- 2 and 9 +/- 2 mm Hg before constriction and by 12 +/- 2 and 12 +/- 4 mm Hg in dogs treated 14 days after renal artery constriction, respectively. Glomerular filtration rate and effective renal plasma flow were unaltered or slightly improved. In sharp contrast, both compounds elicited significant, dose-related decreases in blood pressure (-26 +/- 4 and -20 +/- 4 mm Hg, respectively), glomerular filtration rate (-21 +/- 3 and -23 +/- 3 ml/min), and renal plasma flow (-45 +/- 14 and -48 +/- 13 ml/min) in dogs examined 3 days after renal artery constriction. These data demonstrate that ACHPA-containing renin inhibitory peptide and enalaprilat are equally effective antihypertensive agents in dogs with renin-dependent renovascular hypertension and lend credence to the contention that the renin-angiotensin system supports renal function in hypertensive states in which renin levels are elevated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3028953&dopt=Abstract
Acta Physiol Hung. 1993;81(1):13-8.
Protective effects of the inhibition of the renin-angiotensin system against gastric mucosal lesions induced by cold-restraint in the rat.
Ender F, Labancz T, Rosivall L.
Department of Surgery Schopf-Merei Hospital, Budapest, Hungary.
Experiments were designed to examine whether inhibition of the renin-angiotensin system alters gastric mucosal damage in conscious rats subjected to restraint. Two hours immobilization resulted in an ulcer index of 46 +/- 4 (n = 16) which was decreased by converting enzyme inhibitor (MK 422, enalaprilat) doses of 1 and 10 mg.kg-1.h-1 by 50 +/- 16 (n = 8) and 66 +/- 8% (n = 13), respectively (p < 0.05). Gastric blood flow measured by both the 99Tc-labelled frog erythrocytes and 86Rb-clearance methods was low in untreated rats and increased to more than three-fold in angiotensin converting enzyme inhibitor treated animals. Infusion of saralasin a specific angiotensin II receptor blocker (5 micrograms.kg-1.h-1, n = 25) also decreased the ulcer index by 40 +/- 5% (p < 0.05). Thus inhibition of the renin-angiotensin system in conscious cold-restraint rat increased gastric blood flow and reduced mucosal damage. These results suggest that the renin-angiotensin system plays a significant role in the development of experimental gastric ulcer in the cold-restraint model.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8178650&dopt=Abstract
Hypertension. 1994 Jan;23(1 Suppl):I68-72.
Chronic converting enzyme inhibition facilitates baroreceptor resetting to hypertensive levels.
da Silva VJ, da Silva SV, Salgado MC, Salgado HC.
Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Brazil.
We investigated the acute and chronic effects of converting enzyme inhibitors (captopril or enalapril) and of angiotensin II receptor blockade (DuP 753) on rapid (30-minute) baroreceptor resetting elicited by a prompt and sustained hypertensive response provoked by aortic constriction. Pressure-nerve activity curves, pressure at 50% of maximal baroreceptor activity, baroreceptor gain (slope of the curve), and systolic threshold pressure for baroreceptor activation were determined as indexes of baroreceptor function. A slight fall in mean arterial pressure after acute treatment with the converting enzyme inhibitor or DuP 753 was accompanied by a partial leftward curve shift, which is associated with a partial threshold shift and increase in gain. A maintained hypertensive stimulus caused a partial rightward curve shift and partial (49% to 56%) threshold shift to hypertensive levels in both acutely treated and control rats. The hypertensive stimulus provoked a partial rightward curve shift and complete (88% to 94%) threshold shift to hypertensive levels in chronically treated rats. The effect of enalapril on baroreceptor function was unaltered by the bradykinin antagonist Hoe 140. These data demonstrate that chronic inhibition of converting enzyme or blockade of angiotensin II receptors facilitates rapid resetting of the baroreceptors to hypertensive levels caused by partial aortic constriction without a change in baroreceptor sensitivity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8282378&dopt=Abstract
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