Abstract
The renin-angiotensin and kallikrein-kinin systems play an important role in fetal and neonatal blood pressure control and the circulatory adjustments at birth. Captopril (SQ14,225), a new antihypertensive agent, inhibits angiotensin converting enzyme (ACE). This affects circulating levels of both ACE substrates, angiotensin I and bradykinin (BK). We thought it important to determine whether maternal administration of captopril inhibits fetal ACE activity.
The placenta is the principal site of ACE activity in the fetus (Davidson et al., Circ. Res., in press). We assessed ACE activity on the fetal side of the placenta in situ by perfusing the umbilical artery with Krebs-Hanseleit containing BK 100ng/ml; normal temperature and flow were maintained. ACE activity was defined as the percent of BK (measured by radio-immunoassay) cleared by the placenta after a single passage through the umbilical circulation. The near-term pregnant guinea pig was given 1 mg/kg captopril IV, followed by an infusion of 300 ug/kg/hr for 1 hour. After captopril, fetal ACE activity (20%, SE=6.8, n=7) was significantly less (p <.001) than control activity (77%, SE=2.6, n=12). We conclude that maternal administration of captopril inhibits fetal ACE activity and suggest that the use of captopril in pregnant hypertensive patients could adversely affect blood pressure control in fetal life and during the circulatory adjustments at birth.
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Davidson, D., Stalcup, S. & Mellins, R. 1289 CAPTOPRIL ADMINISTRATION TO THE PREGNANT GUINEA PIG INHIBITS FETAL ANGIOTENSIN CONVERTING ENZYME ACTIVITY. Pediatr Res 15 (Suppl 4), 658 (1981). https://doi.org/10.1203/00006450-198104001-01318
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DOI: https://doi.org/10.1203/00006450-198104001-01318
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