Contribution of different local vascular responses to mid-gestational vasodilation

At-term pregnancy-induced vasodilation is the resultant of endothelium-dependent vasodilation, decreased myogenic reactivity, increased compliance, and reduced sensitivity to vasoconstrictor agents. We hypothesized that these vascular changes are already present at mid-gestation.

In 20 mid-pregnant and 20 nonpregnant Wistar Hannover rats, we measured vascular responses of isolated mesenteric arteries and kidney.

In the pregnant rats compared with the nonpregnant rats, mesenteric flow-mediated vasodilation and renal perfusion flow increased 1.52-fold (from 47±5 to 31±4 μL/min) and 1.13-fold (from 12.8±0.1 to 14.4±0.1 mL/min), respectively. Nitric oxide inhibition reduced mesenteric flow-mediated vasodilation to a similar extent in the pregnant and nonpregnant rats; it completely blocked the pregnancy-induced increase in renal perfusion flow. Pregnancy did not change mesenteric artery sensitivity to phenylephrine, myogenic reactivity, nor vascular compliance.

At mid-gestation, alterations in rat mesenteric vascular tone depend primarily on flow-mediated endothelium-dependent changes and not on changes in α-adrenergic vasoconstrictor sensitivity, myogenic reactivity, or vascular compliance.