CARDIAC ANGIOTENSIN-CONVERTING ENZYME AND ENDOTHELIN RECEPTOR IN RATSWITH CHRONIC MYOCARDIAL-INFARCTION

To ascertain the pathophysiological roles of the renin-angiotensin sys tem and endothelin in heart failure and cardiac hypertrophy we assesse d changes in cardiac angiotensin converting enzyme (ACE) and endotheli n-1 (ET-1) receptor using rats in which myocardial infarction was indu ced by left coronary ligation. The animals were decapitated 1 or 8 mon ths after the operation. Cardiac ACE and ET-I receptor were quantified by computerized in vitro autoradiography using I-125-MK351A (a lisino pril derivative) and I-125-ET-1. One month after myocardial infarction , cardiac weight and plasma atrial natriuretic peptide had increased i n rats with infarction, compared to sham-operated controls, indicating the presence of chronic left ventricular dysfunction, although exchan geable body sodium and plasma renin activity were unchanged. Cardiac A CE increased markedly in the infarcted area and moderately in hypertro phied myocardium without any change in affinity compared to sham-opera ted rats. On the other hand, there was no change in cardiac ET-1 recep tors in infarcted rats. The same results were found even at 8 months a fter myocardial infarction. The present study indicates that cardiac A CE may participate in tissue repair at the site of myocardial infarcti on and may also play a role in the pathophysiology of cardiac hypertro phy in rats with chronic heart failure, However, the present results d o not reveal whether ET-1 receptor participates in the pathophysiology of cardiac hypertrophy in this model.