Captopril에 의한 폐동맥 내피세포중 활성형 Angiotensin 전환효소의 변화

Effects of Captopril on the Active Angiotensin Converting Enzyme at the Pulmonary Endothelial Cells

The effect of captopril on the lung angiotensin converting enzyme (ACE) was investigated after 3 weeks oral administration (120-160 mg/kg/day) through drinking water in Sprague-Dawley rats. On the 125I-351A, an ACE inhibitor, binding assay in the isolated perpused lungs, the number of ACE molecules at the intrapulmonary endothelial cell surface was significantly decreased (p<0.001), and recovered to the normal level 7 days after discontinuation of captopril treatment. Intrapulmonary conversion ratio of AI to AII was also significantly decreased (p<0.05) in the isolated perpused lungs. Bolus intravenous injection of angiotensin I did not showed pressor response in the both of systemic and pulmonary blood pressure of the anesthetized rats. ACE activity of the lung homogenates was also significantly reduced. These data consistently indicate the decrease of functionally active ACE molecule at the pulmonary artery after chronic captopril treatment. However, serum ACE activity was increased three fold in captopril treated rats compared to the normal rats. So, these results suggest that the functionally active ACE molecule at the pulmonary artery was still inhibited, which is directly associated with the antihypertensive effects, even if the total angiotensin converting enzyme induction was resulted after chronic captopril treatment.