The vasoconstrictor response of uterine and mesenteric resistance arteries is differentially altered in the course of pregnancy

Objectives: The purpose of the present study was to test the hypothesis that pregnancy is associated with an attenuation of the vasoconstrictor response not only in the uterine, but also in the systemic circulation. Decreased vascular reactivity should be characterized by an early onset to account for the rapid fall in peripheral resistance which was observed during the first third of gestation. Study design: Dose-response curves for phenylephrine hydrochloride (PE), angiotensin II (ANG II), and endothelin 1 (ET 1) were recorded from isolated pressurized uterine and mesenteric arterioles. Vessels were obtained from virgin, early (day 7–9) pregnant (EP) and late (day 19–21) pregnant (LP) rats. Results: (1) In uterine resistance arteries, the response to PE and ANG II decreased early, but for ANG II the reduction did not persist. ET 1 sensitivity was unchanged in early, and diminished in late gestation; (2) in mesenteric vessels, sensitivity to ET 1 was enhanced in early pregnancy and did not differ from the non-pregnant level in late gestation. Sensitivity to PE and ANG II was unchanged in early, and reduced in late pregnancy. Conclusions: The vasoconstrictor response is not uniformly blunted during pregnancy. Changes in vascular reactivity are differentially regulated with respect to the agonist, to their time course, and. to the origin of the vessel. The relative increase of vasoconstrictor sensitivity in the splanchnic circulation during early pregnancy may prevent hypotensive dysregulation, while concentrations of endogenous vasodilators rise and the vascular filling state normalizes only gradually.