Blood pressure, the renin-aldosterone system and sex steroids throughout normal pregnancy

Abstract Sixty-nine pregnant women were studied sequentially throughout pregnancy and again four to six weeks postpartum. Average blood pressures were lower during pregnancy than postpartum, with diastolic pressures reduced more than systolic pressures. The lowest pressures occurred close to the 28th week of gestation and then tended to return towards nonpregnant levels. Increases in blood pressure that occurred during a change in position from the left lateral recumbent to the supine position did not predict subsequent hypertension in pregnancy; in 51 patients in whom diastolic blood pressure increased by 20 mm Hg or more with this maneuver, hypertension did not develop. Monthly plasma sampling in 19 patients revealed marked stimulation of the renin-aldosterone system, which became maximal in the third trimester. Plasma renin activity (PRA) increased sevenfold over nonpregnant levels. About 50 per cent of this increase could be attributed to an increase in plasma renin substrate. Mean plasma renin substrate increased by fourfold, plasma aldosterone by eightfold, whereas urinary aldosterone excretion increased even more. Both urine and plasma aldosterone correlated with increasing PRA. Plasma progesterone, estradiol and estriol also progressively increased throughout pregnancy and were correlated closely with each other. Altogether, these studies describe an early and sustained stimulation of the renin-aldosterone system in normal pregnancy that is independent of changes in sodium or potassium excretion. The increases observed in PRA are of lesser magnitude and are more consistent throughout pregnancy in individual subjects than previously reported, perhaps because inadvertent cryoactivation of inactive renin was avoided prior to renin measurement. Increases in the renin system activity in pregnancy very likely involve increased stimulation of renal renin secretion consequent to hemodynamic and fluid volume changes which tend to compromise effective arterial blood volume and pressure. These data provide base line patterns for study of the pathogenesis of hypertensions and toxemias of pregnancy.