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The ontogeny of human pulmonary angiotensin‐converting enzyme and its aberrant expression may contribute to the pathobiology of bronchopulmonary dysplasia (BPD)

The mammalian lung possesses the highest level of angiotensin converting enzyme (ACE) amongst all the organs. ACE is known to generate angiotensin (AT)‐II from AT‐I and to regulate serum bradykinin level, thereby controlling blood pressure. Recent data, however, indicate a role for ACE derived AT‐II in angiogenesis, pulmonary hypertension, and neonatal lung disease. The ontogeny of ACE in humans has not been investigated. We studied pulmonary ACE expression during human lung development and in human bronchopulmonary dysplasia (BPD).