Hypoxia simulated to high altitude promotes right ventricular ACE2 activity in adult SD rats independent of pulmonary artery hypertension

AIM: To determine the right ventricular angiotensin converting enzyme2 (ACE2) activity in adult SD rats under normoxia and hypoxia environment, and to detect the relationship between ACE2 and high altitude heart disease initially. METHODS: Adult male Sprague Dawley (SD) rats were raised under hypoxia environment simulated to high altitude (5 000 m, 23 h/d), then divided into hypoxia 1 d, 15 d and 30 d groups randomly. The control group was set up under normoxia environment. The right ventricular function, ponderal index, pulmonary artery pressure and right ventricular ACE2 activity were determined. The effect of captopril or nitrendpine on cardiac ACE2 activity in hypoxia 30 d group was also observed. RESULTS: The dramatic up-regulation of cardiac ACE2 expression of mRNA and protein and its activity in hypoxia 30 d group was observed, together with obvious increase in right ventricular function, ponderal index and pulmonary artery pressure. Although captopril or nitrendipine depressed pulmonary artery pressure and cardiac function dramatically, no significant alteration of right ventricular ACE2 activity was detected. CONCLUSION: Chronic hypoxic exposure promotes the ACE2 expression and activity in right ventricular, indicating that ACE2 may be correlated to the changes of cardiac architecture and function induced by hypoxia. Up-regulation of ACE2 expression maybe contribute to the increase in right ventricular ACE2 activity, and pulmonary artery hypertension may not be the main reason for the changes of ACE2 activity under hypoxia environment.