Angiotensin-converting enzyme activity and its modulation by oxygen tension in the guinea pig fetal-placental unit.

Publisher Website
Google Scholar
Abstract
Angiotensin-converting enzyme (ACE) activity in the guinea pig fetal-placental unit was assessed at the different O2 tensions found in utero, during labor and at birth. To determine fetal-placental ACE activity, in situ term guinea pig fetuses and their placentas were perfused via the umbilical vessels under controlled conditions of flow, temperature and pH. ACE activity was defined as the percent of angiotensin I (AI) or bradykinin (BK) in Krebs-Henseleit solution cleared by a single passage through the placenta or fetus. Peptide concentrations were measured by radioimmunoassay (RIA). Using BK as substrate, placental and fetal ACE activities were reflected by 45% (SD = 10) and 24% (SD = 7) clearances, respectively, at a perfusate PO2 [partial pressure of O2] of 29 mm Hg. Maternal hypoxia (PaO2 [arterial PO2] = 28 mm Hg) decreased placental ACE activity to 16% (SD = 8) and maternal hyperoxia (PaO2 = 191 mm Hg) increased placental ACE activity to 56% (SD = 9). Using a perfusate PO2 of 95 mm Hg, fetal and placental ACE activity increased in less than 5 min to 75% (SD = 10) and 77% (SD = 9), respectively. Similar results were obtained using AI as substrate. Fetal-placental ACE activity exhibits a chronically reduced level of activity appropriate to the low O2 tension found in the fetal-placental unit; the placenta is the primary site of ACE activity in the fetus; maternal oxygenation modulates fetal-placental ACE activity; and fetal ACE activity acutely increases with increased fetal oxygenation and thus may play an important physiological role in the regulation of circulating levels of BK and AII and the circulating adjustments at birth.