Disproportionate decrease in alpha- compared with beta-adrenergic sensitivity in the dorsal hand vein in pregnancy favors vasodilation.

Abstract

Altered vascular responses to adrenergic agonists during pregnancy are thought to play an important role in the regulation of blood pressure and placental blood flow. Because alpha1-adrenergic and beta2-adrenergic sensitivity act in opposing directions to determine vascular tone, we simultaneously evaluated alpha-adrenergic-mediated vasoconstriction and beta-adrenergic-mediated vasodilation in dorsal hand veins during and after pregnancy. Twenty healthy pregnant women were studied at 32 to 37 weeks of gestation and again 12 weeks after delivery. Vascular response to phenylephrine (PE) and isoproterenol (ISO) was measured in a dorsal hand vein using the linear variable differential transformer technique. The dose of PE resulting in 50% constriction (CD50) was determined. The response to ISO was measured after the PE preconstriction. Pregnant and postpartum values, expressed as geometric mean (95% CI), were compared by paired t test. alpha-Adrenergic sensitivity during pregnancy (CD50 2.7 micro g/min [95% CI, 1.5 to 5.0]) was markedly decreased, approximately 7-fold, compared with postpartum (0.4 micro g/min [95% CI, 0.3 to 0.7] [P<0.01]). beta-Adrenergic vasodilation was also attenuated during pregnancy. The ED50 of ISO (dose of ISO resulting in 50% of the maximal response, E(max)) was greater during pregnancy (20 ng/min [95% CI, 11 to 35]) than postpartum (8 ng/min [95% CI, 5 to 12]) (P<0.05). ISO E(max) was also significantly less during pregnancy (81% [95% CI, 65 to 97] compared with postpartum (105% [95% CI, 97 to 113]) (P<01.01). Normal pregnancy is characterized by decreased venous sensitivity to both alpha1-adrenoceptor-mediated vasoconstriction and beta2-adrenoceptor-mediated vasodilation. The greater decrease in alpha1 compared with beta2 response may contribute to the vasodilated state characteristic of human pregnancy.