Effect of pregnancy on contraction and endothelium-mediated relaxation of renal and mesenteric arteries.

We have hypothesized that differences in the effect of pregnancy on mechanisms modulating vascular reactivity underlie the redistribution of cardiac output. Because pregnancy increases mesenteric blood flow by 75% and renal blood flow by only 10% in the guinea pig, we investigated the effect of pregnancy on vascular reactivity in these two beds. Relaxation in response to acetylcholine (ACh), an endothelium-dependent relaxing agent, and contraction induced by the thromboxane mimetic U-46619 were measured in ring segments of mesenteric and renal arteries from pregnant and nonpregnant guinea pigs. To determine the role of the endothelium, nitric oxide (NO), and vasodilator prostaglandins in modulating vascular response, rings were denuded, treated with N omega-nitro-L-arginine (L-NNA) to inhibit NO synthase, or treated with indomethacin to inhibit cyclooxygenase. Pregnancy increased ACh-stimulated relaxation of mesenteric arteries but not renal arteries. L-NNA significantly reduced ACh sensitivity (based on the concentration that produced 50% of the maximal response) in arteries from pregnant and nonpregnant animals, and indomethacin slightly decreased maximal relaxation only in the renal artery of nonpregnant animals. ACh sensitivity of mesenteric arteries was still increased after L-NNA or indomethacin. Pregnancy reduced the threshold concentration of U-46619 in mesenteric artery but had no effect on contraction of renal artery. Contraction of both arteries was enhanced by denudation. L-NNA and indomethacin were less effective than denudation in arteries from pregnant and nonpregnant animals, which suggests that pregnancy alters thromboxane contraction by endothelium-dependent mechanisms other than NO and prostaglandins. Thus, pregnancy differentially alters vascular reactivity of mesenteric and renal arteries in the guinea pig.