Mechanisms Underlying Maternal Venous Adaptation in Pregnancy

To define the effects of pregnancy on mechanical properties and reactivity, mesenteric veins from late pregnant and virgin control (nonpregnant) rats were pressurized to determine gestational changes in size and distensibility. Reactivity studies used an adrenergic constrictor (norepinephrine) and an endothelium-mediated vasodilator (acetylcholine). The contribution of nitric oxide to endothelial function was evaluated with pharmacologic inhibition of nitric oxide synthase. Roles of nitric oxide and cyclic guanosine monophosphate in smooth muscle vasodilation were determined using an nitric oxide donor with and without cyclic guanosine monophosphate inhibition using ODQ, a selective inhibitor of guanylyl cyclase. In pregnancy, endothelium-dependent vasodilation markedly increased (largely due to endogenous nitric oxide), smooth muscle response to nitric oxide decreased (primarily related to cyclic guanosine monophosphate production), and norepinephrine sensitivity decreased considerably, with no changes in vessel size or distensibility. Our results identify a provasodilatory state in the systemic venous system, which would serve to facilitate the accommodation to plasma volume expansion requisite normal pregnancy.