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Angiotensin-II sensitivity and prostaglandin-synthetase inhibition in pregnancy
Angiotensin-II sensitivity was measured with a standardized test in 8 healthy nonpregnant females and in 14 healthy primigravid women. In the primigravid women the effective pressor dose (EPD), i.e. the minimal dose of angiotensin-II (A-II) necessary for a rise in diastolic blood pressure of 20 mm Hg, was 17.1 +/- 5.7. This is significantly higher than the EPD in the control group (5.2 +/- 1.2). The pregnant patients were also tested 75 min after a 50 mg indomethacine suppository, which produced a decrease of the EPD of 9.5 +/- 3.0, a fall of 44%. None of the 7 patients tested between 28 and 32 wk of gestation developed pregnancy-induced hypertension. They all had a normal EPD. It may be concluded that (1) A-II sensitivity is decreased in pregnancy, and (2) vascular reactivity in pregnancy is at least in part mediated by prostaglandins.
Angiotensin-II sensitivity was measured with a standardized test in 8 healthy nonpregnant females and in 14 healthy primigravid women. In the primigravid women the effective pressor dose (EPD), i.e. the minimal dose of angiotensin-II (A-II) necessary for a rise in diastolic blood pressure of 20 mm Hg, was 17.1 +/- 5.7. This is significantly higher than the EPD in the control group (5.2 +/- 1.2). The pregnant patients were also tested 75 min after a 50 mg indomethacine suppository, which produced a decrease of the EPD of 9.5 +/- 3.0, a fall of 44%. None of the 7 patients tested between 28 and 32 wk of gestation developed pregnancy-induced hypertension. They all had a normal EPD. It may be concluded that (1) A-II sensitivity is decreased in pregnancy, and (2) vascular reactivity in pregnancy is at least in part mediated by prostaglandins.