Parturition Alters Estrogen Signaling in Microvascular Arteries: Impaired nNOS

Estrogen (E2) levels normally decline after parturition; however, many women artificially increase estrogen levels after pregnancy by taking oral contraceptives. Little is known regarding how parturition affects estrogen signaling, especially in the microvasculature, which is a major determinant of blood pressure. Our hypothesis was that parturition attenuates E2‐induced relaxation in mesenteric arteries by decreasing NO production. We found that microvessels from postpartum animals exhibited: 1) unaltered contractility to phenylephrine, 2) enhanced relaxation response to acetylcholine (79.76 ± 8.26% vs nulliparous controls 57.83 ± 9.34% relaxation), 3) endothelium‐independent, E2‐induced relaxation (intact 18.78 ± 3.84% vs denuded 15.37 ± 3.30%), 4) impaired E2‐induced relaxation due to decreased NOS activity (L‐NMMA, −17.54 ± 15.66% vs postpartum controls 12.98 ± 2.94% relaxation at 1000nM E2), 5) impaired nNOS‐dependent, E2‐induced relaxation, and 6) decreased nNOS expression. Thus, these data indicate that estrogen‐induced relaxation of microvascular arteries is depressed in postpartum animals due to decreased expression of nNOS in vascular smooth muscle. HL073890