Abstract
The usefulness of angiotensin converting enzyme (ACE) inhibitor in the treatment of congestive heart failure is well known. In order to study the effect of ACE inhibitor on compensatory cardiac hypertrophy and failure, captopril, a potent ACE inhibitor, was administered to experimental myocardial infarction (MI) rats.
The systolic blood pressure was significantly lowered and the left ventricular end-diastolic pressure was lowered in captopril-treated MI rats. Both the left and right ventricular weight/body weight ratios were significantly greater in non-treated MI rats than in controls and captopril-treated MI rats, while there were no significant differences between the latter two groups.
Percent V3 myosin heavy chain was increased in non-treated MI rats, but this increase was obviously suppressed by administration of captopril for 4 weeks. β-MHC mRNA expression determined by northern blotting analysis was also distinctly lower in 1 week treated rats than in non-treated MI rats. The plasma atrial natriuretic peptide (ANP) concentration andγ-rANP mRNA expression were significantly lower in captopril-treated MI rats than in non-treated MI rats.
Thus, captopril induced regression of cardiac hypertrophy, reversed the cardiac MHC profile and improved hemodynamic alterations in experimental MI rats. The present results further suggest that not only afterload reduction but also preload reduction may be responsible for the beneficial effects of captopril in cardiac hypertrophy and failure.
