Angiotensin-Converting Enzyme Inhibition and Salt in Experimental Myocardial Infarction

It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether...

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Veröffentlicht in:Journal of cardiovascular pharmacology 1998-09, Vol.32 (3), p.357-365
Hauptverfasser: Yoshida, Kazunori, Kohzuki, Masahiro, Casley, David J, Johnston, Colin I
Format: Artikel
Sprache:eng
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Zusammenfassung:It is well known that angiotensin-converting enzyme inhibitors attenuate progressive ventricular enlargement or hypertrophy after myocardial infarction and that cardiac angiotensin-converting enzyme activity is increased in the rat model of myocardial infarction. In this study, to determine whether the beneficial effects of angiotensin-converting enzyme inhibition on cardiac hypertrophy after myocardial infarction are due to a reduction in ventricular afterload or to inhibition of cardiac angiotensin-converting enzyme, we used sodium loading during angiotensin-converting enzyme inhibition. The rat model of myocardial infarction was treated with a vehicle, 1% saline, as drinking fluid, perindopril (2 mg/kg/day), or 1% saline as drinking fluid plus perindopril (2 mg/kg/day) for 6 weeks. Perindopril reduced blood pressure, prevented cardiac hypertrophy, and inhibited cardiac angiotensin-converting enzyme. The effects of perindopril on blood pressure and cardiac hypertrophy 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 reduction than on cardiac angiotensin-converting enzyme inhibition in the rat model of myocardial infarction.
ISSN:0160-2446
1533-4023
DOI:10.1097/00005344-199809000-00004