INCREASED PLATELET ANGIOTENSIN-II RECEPTOR NUMBER IN PREGNANCY-INDUCED HYPERTENSION

Women with pregnancy-induced hypertension (PIH) are characterized by relatively greater blood pressure sensitivity to exogenous angiotensin II (Ang II) than normotensive pregnant women. Evidence suggests that this is due to an alteration in Ang II receptor sites. However, the question of whether this represents an increase in receptor number or affinity remains unanswered. To answer this question Ang II receptors on platelets from normotensive women during each trimester of pregnancy and the postpartum period were studied and compared with platelet Ang II binding in third trimester women with PIH and in postpartum women who had had a recent pregnancy complicated by PIH. We also measured plasma renin activity, Ang II, and aldosterone in blood samples from these women and sodium and creatinine in 24-hour urine collections. Normotensive pregnant women had significantly less platelet Ang II binding than nonpregnant, postpartum women (0.85+/-0.19 versus 2.87+/-0.83%, p=0.003), reflecting a reduction in receptor number but not affinity. This probably reflects the significant increase in Ang II during pregnancy. Urinary sodium excretion was equivalent and could not explain these changes. Comparisons of third trimester women with PIH against those without PIH documented a significantly higher Ang II binding in the women with PIH (2.23+/-0.42 versus 0.85+/-0.19%) that was caused by an increase in receptor number (6.0+/-1.3 versus 3.0+/-0.8 fmol Ang II per 5.6 x 10(8) platelets, p=0.047) but similar Ang II binding affinity. This reflected significantly lower Ang II levels. There was no difference in urinary sodium excretion between the groups. In the postpartum period there were no differences in Ang II receptor binding and plasma hormone levels between women with previously normotensive versus hypertensive pregnancies. These results suggest that the enhanced Ang II sensitivity found in pregnant women with PIH is due to increased Ang II receptor number, which reflected relative reductions in Ang II levels.