K. Yoshida et al., ANGIOTENSIN-CONVERTING ENZYME-INHIBITION AND SALT IN EXPERIMENTAL MYOCARDIAL-INFARCTION, Journal of cardiovascular pharmacology, 32(3), 1998, pp. 357-365
It is well known that angiotensin-converting enzyme inhibitors attenua
te progressive ventricular enlargement or hypertrophy after myocardial
infarction and that cardiac angiotensin-converting enzyme activity is
increased in the rat model of myocardial infarction. Tn this study, t
o determine whether the beneficial effects of angiotensin-converting e
nzyme inhibition on cardiac hypertrophy after myocardial infarction ar
e due to a reduction in ventricular afterload or to inhibition of card
iac angiotensin-converting enzyme, we used sodium loading during angio
tensin-converting enzyme inhibition. The rat model of myocardial infar
ction was treated with a vehicle, 1% saline, as drinking fluid, perind
opril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (
2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevente
d cardiac hypertrophy, and inhibited cardiac angiotensin-converting en
zyme. The effects of perindopril on blood pressure and cardiac hypertr
ophy were abolished by sodium loading, which did not alter the degree
of cardiac angiotensin-converting enzyme inhibition. Thus the actions
of perindopril on cardiac hypertrophy depend more on blood pressure re
duction than on cardiac angiotensin-converting enzyme inhibition in th
e rat model of myocardial infarction.