COMPARISON OF ANGIOTENSIN-CONVERTING ENZYME AND RENIN INHIBITION IN RATS FOLLOWING MYOCARDIAL-INFARCTION

Citation
Pf. Mento et al., COMPARISON OF ANGIOTENSIN-CONVERTING ENZYME AND RENIN INHIBITION IN RATS FOLLOWING MYOCARDIAL-INFARCTION, Journal of cardiovascular pharmacology, 21(5), 1993, pp. 791-796
Citations number
23
Categorie Soggetti
Cardiac & Cardiovascular System","Respiratory System","Pharmacology & Pharmacy
ISSN journal
01602446
Volume
21
Issue
5
Year of publication
1993
Pages
791 - 796
Database
ISI
SICI code
0160-2446(1993)21:5<791:COAEAR>2.0.ZU;2-4
Abstract
Renal and systemic hemodynamics were studied in rats 1 month after ind uction of myocardial infarction by ligation of the left coronary arter y. The mean arterial pressure, heart rate, and cardiac index were not different from controls, but there were striking elevations in heart w eight (p < 0.001), left ventricular end diastolic pressure (p < 0.002) , and renal vascular resistance (p < 0.01). Renal blood flow and the p ercent of cardiac output perfusing the kidneys were reduced by 18% (p < 0.01) and 14% (p < 0.01), respectively. Acute angiotensin inhibition was studied at a dose of the converting enzyme inhibitor, enalapril, or the renin inhibitor, CP71362, that lowered the mean arterial pressu re by 15 mm Hg in normal rats. In normal rats, enalapril and CP71362 w ere without effect on renal blood flow (RBF), renal vascular resistanc e (RR), and RBF as a percent of cardiac output. However, in rats with myocardial infarction, enalapril and CP71362 increased the RBF and RBF as a percent of cardiac output and lowered the RR to levels similar t o normal controls (p < 0.02). Enalapril and CP71362 were equally effec tive in reducing the left ventricular end-diastolic pressure and total peripheral resistance in rats with myocardial infarction. These data demonstrate significant intrarenal vasoconstriction following myocardi al infarction in the absence of detectable changes in mean arterial pr essure or cardiac index. Converting enzyme inhibition or renin inhibit ion had similar beneficial effects on cardiorenal function, suggesting that both classes of compounds act by a similar mechanism to improve renal hemodynamics in congestive heart failure.