P.N. Baker

Platelet angiotensin II binding sites in normotensive and hypertensive women

Summary. Specific binding of angiotensin II (AII) to platelets was measured in 89 women, 25 nulliparous non‐pregnant women and 64 primigravida in the third trimester of pregnancy. There was significantly lower binding in the 25 pregnant women who were normotensive (2.3 fmol/109 cells) when compared with the non‐pregnant women (9.0 fmol/109 cells P<0.001). Significantly higher platelet AII binding levels were found in the 39 women who had pregnancy induced hypertension (PIH) (5.5 fmol/109 cells) when compared with the 25 normotensive pregnant women (P<0.001). Of the 39 women with PIH, platelet AII binding was higher in the 23 women who had pre‐eclampsia (7.0 fmol/109 cells), when compared with the 16 who had non‐proteinuric PIH, (4.6 fmol/109 cells) although the difference was not statistically significant (P<0.04). The pressor response to AII is also diminished in pregnancy, yet less so if pregnancy induced hypertension develops. Platelets may provide a readily accessible tissue with which to study AII responsiveness in pregnancy.

Angiotensin II Has Depressor Effects in Pregnant and Nonpregnant Women

Studies in anesthetized animals suggest that angiotensin II evokes a depressor as well as a pressor effect, which becomes evident on cessation of infusion. We have studied 18 nonpregnant and 8, 23, and 22 women in the first, second, and third trimesters of pregnancy to determine whether such an effect is present in conscious women, whether it is dose dependent, and whether it is influenced by pregnancy. Angiotensin II was infused intravenously in doubling concentrations at 10-minute intervals until a pressor effect of approximately 20 mm Hg was observed. The infusion was stopped, and blood pressure was monitored at 2-minute intervals for 30 minutes. There was a significant diastolic depressor effect after stopping angiotensin II in the nonpregnant women and those in the second and third trimesters of pregnancy. Individual women required differing doses of angiotensin II to evoke the standardized pressor response. It was thus possible to examine the depressor response in each group in relation to infused doses of angiotensin II. In nonpregnant women and in those in the second and third trimesters of pregnancy, the depressor response was dose dependent (P<.001). At any given dose, the depressor response deepened as pregnancy progressed (P<.001). Basal plasma prostacyclin concentrations rise in pregnancy, and angiotensin II can stimulate prostacyclin synthesis. This might mediate the depressor effect. In conclusion, the diminished pressor response to angiotensin II in normal pregnancy may be partly due to an increasing depressor effect of the hormone.

Abdominal pain of unknown aetiology in pregnancy

Summary. The outcome of 140 pregnancies complicated by unexplained abdominal pain was compared with that in a comparison group of 280 women who gave birth at the same time. The two groups were comparable for maternal age and parity but the study group contained a significantly higher proportion of smokers, unmarried women, and women whose partners were unemployed (P<0·001). All the pregnancies resulted in livebirths. There were no statistically significant differences in birthweight, gestational age at delivery or mode of delivery between the two groups.