A study of angiotensin II pressor response throughout primigravid pregnancy

The present study was designed to ascertain sequentially the pressor response to angiotensin II in young primigravid patients throughout pregnancy in order to define when in pregnancy resistance to the pressor effects of angiotensin II develops; to define the physiologic sequence of events leading to this resistance; and to ascertain whether sensitivity to infused angiotensin II could be detected before the onset of clinical signs of pregnancy induced hypertension. With this prospective approach, 2 separate groups of patients were defined. The first group of patients remained normal throughout pregnancy. The second group consisted of those patients who, while clinically normotensive during the initial phase of the study, ultimately developed hypertension of pregnancy. 192 patients were studied; of these, 120 patients remained normotensive and 72 developed pregnancy induced hypertension. In both groups, vascular resistance to infused angiotensin II (more than 8 ng/kg/min required to elicit a pressor response of 20 mm Hg in diastolic pressure) was demonstrated as early as the 10th wk of pregnancy. In the group that remained normotensive, maximum mean vascular resistance occurred at 18-30 wk of pregnancy (mean pressor dose required being 13.5 to 14.9 ng/kg/min). In those subjects who developed pregnancy induced hypertension, the mean maximum dose required was 12.9 ng/kg/min, which was observed at the 18th wk of pregnancy. By the 22nd wk there was a clear separation of the 2 groups, with the mean dose requirement of the subjects destined to develop hypertension being progressively less than that of those who remained normal. The difference between the 2 groups became significant (P<0.01) by 23-26 wk of pregnancy. Among patients requiring more than 8 ng/kg/min on one or more tests done between wk 28-32, 91% remained normotensive. Conversely, during the same time period among patients requiring less than 8 ng/kg/min, on at least one occasion, 90% developed pregnancy induced hypertension.