Greater stimulated and basal release of nitric oxide in the presence of estradiol

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FASEB Journal







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We recently reported that acute administration of 17-β-estradiol (1-30 uM) a) stimulated whole-cell K-currents of rabbit aortic endothelial cells studied under whole-cell clamp, and b) increased intracellular free Ca levels in single endothelial cells and the intact endothelial preparation of rabbit cardiac valves (BBRC, 214,367,1995). In this study, we report on the modulatory effects of estradiol on the release of nitric oxide in rings of rat aorta studied under isometric conditions. Dilator responses to acetylchoUne (Ach, lOnM10 μM) were obtained in phenylephrine (PE, 10 μM) contracted aorta, and constrictor dose-response curves to PE (1 nM-10 μM) were made before and after pretreatment with L-NNA (200 μM), an inhibitor of nitric oxide synthase. Tissue segments were obtained from three groups of age-matched rats:- i) sham-operated, vehicle treated, ii) overiectomized,vehicle treated and iii) overiectomized, estradiol treated (0.1 mg/kg/day, P.O., 35 days). Aortic rings from sham and overiectomized rats receiving estradiol a) were more sensitive to the dilator effects of Ach, b) constricted less to PE in the absence of L-NNA and c) had a greater potentiation of the PE responses after inhibition of nitric oxide synthase. These findings are in agreement with our previous report and show that treatment with estradiol enhances endothelial secretion of nitric oxide.

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