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
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.