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Estrogen‐induced resistance artery relaxation is nNOS‐ and age‐dependent in postpartum rats
Author(s) -
Royal Crista,
White Richard
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.588.4
Subject(s) - vasodilation , mesenteric arteries , endocrinology , medicine , nitric oxide , estrogen , isometric exercise , artery , nitric oxide synthase , blood vessel , uterine artery , vascular resistance , pregnancy , hemodynamics , biology , gestation , genetics
Our hypothesis is that pregnancy and parturition alter how resistance vessels respond to the vasoactive hormone 17β‐estradiol (E2). We performed isometric contractile force recordings on mesenteric resistance arteries from female Sprague Dawley rats. Normally, E2 is a vasodilator. We found that relaxation to E2 was impaired in younger (≤19 weeks old) postpartum rats as compared to age‐matched nulliparous, or virgin, controls. Arteries from animals older than 20 weeks exhibited no significant impairment. We had previously demonstrated that E2 relaxes arterial smooth muscle by stimulating nitric oxide production from neuronal nitric oxide synthase (nNOS) expressed in vascular smooth muscle. Pretreating vessels with 10 −4 M L‐NPA, a nNOS selective inhibitor, inhibited E2‐induced relaxation arteries from control rats by 102.17±6.12%, and by 93.65±3.11% in arteries from older postpartum animals. In contrast, L‐NPA had no effect on arteries from younger postpartum animals that exhibit impaired relaxation. These findings suggest that dysfunction of normal nNOS‐mediated relaxation may contribute to the diminished responsiveness of mesenteric microvessels from young postpartum rats to E2. HL073890