Estrogen signaling alterations in resistance arteries postpartum (849.6)

Few studies have examined the after‐effects of childbirth on the female vasculature – especially the resistance microvasculature of non‐reproductive tissues, which are a major determinant of blood pressure. 17β‐estradiol (E2), an important vasoactive hormone, normally declines after parturition; however, many women artificially increase estrogen levels after pregnancy by taking oral contraceptives. Our hypothesis was that parturition attenuates E2‐induced relaxation in mesenteric arteries by decreasing nNOS expression. We measured a 73% decrease in serum E2 levels in the postpartum state compared to nulliparous Sprague‐Dawley rats. We found that microvessels from postpartum animals exhibited: 1) endothelium‐independent, E2‐induced relaxation (intact 18.78 ± 3.84% vs denuded 15.37 ± 3.30%), 2) 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), 3) impaired nNOS‐dependent, E2‐induced relaxation, and 4) decreased nNOS expression (down 39% p=0.0077). Because E2 has been shown to increase nNOS protein expression, we propose that lower E2 levels after parturition decrease expression of nNOS, leading to a reduced vasodilatory capacity of resistance microvessels. Grant Funding Source : Supported in part by NIH HL073890