[Effect of captopril on the activities of angiotensin II and angiotensin converting enzyme during hypoxia induced pulmonary hypertension].

To evaluate the role of angiotensin system in the development of hypoxia induced pulmonary hypertension, nine pigs (50 +/- 8 kg) were studied. A Swan-Ganz Catheter and an arterial catheter were inserted into the pulmonary artery and aorta. Pulmonary arterial pressure (PAP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO) and arterial blood gases were monitoring before and after hypoxia and captopril injection (7.0 mg/kg). Plasma renin activity (PRA) and angiotensin II (ATII) were measured by RIA. Angiotensin converting enzyme (ACE) by fluorometry. Results showed during hypoxemia (PaO2 6.2 +/- 0.3 kPa, PaCO2 5.3 +/- 0.2 kPa): PAP increased from 2.4 +/- 0.2 to 3.8 +/- 0.3 kPa, (P less than 0.05) and right ventricle stroke work index (RVSWI) from 55.7 +/- 7.2 to 91.3 +/- 9.3 mJ/m2 (P less than 0.05); mean-while PRA increased from 0.6 +/- 0.2 to 1.3 +/- 0.3 mol.L-1/h (P less than 0.05) and ATII from 62.4 +/- 17.2 to 133.3 +/- 31.8 ng/L (P less than 0.01). But ACE decreased from 77.6 +/- 5.2 to 58.4 +/- 4.2 mumol.min-1/L (P less than 0.05). After Captopril injection ACE was remarkably reduced to 26.7 +/- 3.4 mumol.min-1/L (P less than 0.001) and ATII dropped to 61.9 +/- 15.5 ng/L (P less than 0.01) compared with those during hypoxemia. There was significant correlation between PAP and PRA (r = 0.564, P less than 0.01). We speculate that angiotensin system may play a part in acute hypoxia induced pulmonary hypertension and captopril inhibits the production of ATII leading to the decrease of pulmonary arterial pressure.