Flow-mediated vasodilatation is enhanced in normal pregnancy but reduced in preeclampsia.

Endothelium-derived nitric oxide is proposed to play an important role in the lowering of peripheral vascular resistance in normal pregnancy. In women with preeclampsia, the function of the endothelium is compromised, and it is suggested that reduced nitric oxide synthesis may contribute to the elevation of blood pressure and activation of coagulation pathways. In this study, we have compared responses to increments of intraluminal flow, considered to be a physiological stimulus to nitric oxide release, in arteries from normotensive nonpregnant and pregnant women and women with preeclampsia. Small subcutaneous arteries from normotensive pregnant women showed substantial flow-induced relaxation, which was attenuated by the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) (mean relaxation, 48.3+/-8.0% [absence of L-NAME] versus 19.2+/-10.6% [presence of L-NAME]), whereas those from nonpregnant women and women with preeclampsia demonstrated modest constriction (mean constriction, 10.1+/-7.3% and 1.2+/-7.2%, respectively). Shear stress, the frictional force that is the stimulus for flow responses, was calculated from parameters of flow, viscosity, and artery diameter. Arteries from pregnant women showed greater relaxation to shear than those from nonpregnant women or those with preeclampsia. We conclude that flow-induced shear stress is a potent stimulus to vasodilatation in arteries from pregnant women and that this mechanism may lead to a fall in peripheral vascular resistance in normal pregnancy. Failure of this flow-induced dilatation may contribute to the gestational hypertension of preeclampsia.