ACUTE EFFECTS OF CAPTOPRIL, AN ANGIOTENSIN-CONVERTING ENZYME-INHIBITOR, ON THE PREGNANT EWE AND FETUS

After control measurements had been made, 15 chronically catheterized pregnant ewes (gestational age 123-141 days) were given 15 mg of captopril intravenously followed by an infusion of 6 mg/h. These doses blocked the pressor responses of both ewes and fetuses to 5-mu-g of angiotensin I. After captopril, maternal mean arterial pressure fell from 94 +/- 3.5 to 88 +/- 3.6 (SE) mmHg (P < 0.0001) and pulse interval fell (P = 0.008). Maternal flow to the cotyledons fell from 766 +/- 118 to 525 +/- 77 ml/min (P = 0.002), as did flow to the remainder of the maternal placenta, i.e., the caruncles and their underlying myoen-dometrium (control flow 188 +/- 35 ml/min, flow 10-15 min after captopril 166 +/- 36.1 ml/min; P = 0.021). Flow to the rest of the myometrium did not change. Fetal arterial pressure fell from 46.9 +/- 1.6 to 44.1 +/- 1.6 mmHg (P < 0.009), and fetal placental blood flow fell from 639.9 +/- 93.2 to 413.1 +/- 53.9 ml/min (P = 0.025). Flow to the fetal membranes declined also, from 53.2 +/- 6.5 to 35.6 +/- 3.3 ml/min (P < 0.005). Maternal and fetal renal blood flows and fetal adrenal blood flows were unchanged. Fetal arterial PO2 was initially 19.5 +/- 0.8 mmHg; after captopril, it was 17.7 +/- 0.9 mmHg (P = 0.03). Fetal urine flow rate fell from 0.66 +/- 0.08 ml/min to nadir of 0.25 +/- 0.08 ml/min (P < 0.0001) while urinary osmolality rose from 108 +/- 5 mosmol/kgH2O to a maximum of 229 +/- 42 mosmol/kgH2O at the end of the experiment (P = 0.001). Sodium excretion (P = 0.022) also declined from 15.8 +/- 2.6 to 8.8 +/- 1.7-mu-mol/min. It is concluded that captopril induces maternal hypotension and falls in maternal and fetal placental flows, which leads to changes in fetal blood gases and fetal renal function. However, there may also be direct effects of captopril on fetal renal function.