OBJECTIVE: To clarify the physiologic function of angiotensin-converting enzyme (EC 3.4.15.1) in the human placenta. METHODS: The concentrations of angiotensin I and angiotensin II were measured in the umbilical artery and vein. In addition, the expression of angiotensin-converting enzyme messenger RNA (mRNA) and its activity in the human placenta were studied. The amount of angiotensin-converting enzyme mRNA was measured by Northern blot hybridization with specific human complementary DNA. RESULTS: The mean (+/- standard deviation) level of angiotensin I was significantly higher in the umbilical artery than in the umbilical vein (1044.5 +/- 626.5 versus 796.5 +/- 372.8 pg/mL; P < .05). In contrast, the mean level of angiotensin II was significantly lower in the umbilical artery than in the umbilical vein (97.3 +/- 102.9 versus 129.3 +/- 110.3 pg/mL; P < .05). Angiotensin-converting enzyme mRNA was detected in the human placenta at 4.5 and 3.9 kilobases. The amount of angiotensin-converting enzyme mRNA increased over the course of pregnancy but decreased near term, whereas angiotensin-converting enzyme activity in the human placenta continued to increase from the first trimester to term. CONCLUSION: The placenta appears to contribute to the conversion of angiotensin I to angiotensin II in the fetal circulation.
OBJECTIVE: To clarify the physiologic function of angiotensin-converting enzyme (EC 3.4.15.1) in the human placenta. METHODS: The concentrations of angiotensin I and angiotensin II were measured in the umbilical artery and vein. In addition, the expression of angiotensin-converting enzyme messenger RNA (mRNA) and its activity in the human placenta were studied. The amount of angiotensin-converting enzyme mRNA was measured by Northern blot hybridization with specific human complementary DNA. RESULTS: The mean (+/- standard deviation) level of angiotensin I was significantly higher in the umbilical artery than in the umbilical vein (1044.5 +/- 626.5 versus 796.5 +/- 372.8 pg/mL; P < .05). In contrast, the mean level of angiotensin II was significantly lower in the umbilical artery than in the umbilical vein (97.3 +/- 102.9 versus 129.3 +/- 110.3 pg/mL; P < .05). Angiotensin-converting enzyme mRNA was detected in the human placenta at 4.5 and 3.9 kilobases. The amount of angiotensin-converting enzyme mRNA increased over the course of pregnancy but decreased near term, whereas angiotensin-converting enzyme activity in the human placenta continued to increase from the first trimester to term. CONCLUSION: The placenta appears to contribute to the conversion of angiotensin I to angiotensin II in the fetal circulation.