BACKGROUND AND PURPOSE: It has been reported that estrogens modulate peripheral vascular synthesis of vasodilatory hormones, including prostacyclin. If this occurs in the cerebral circulation, it could have important consequences in the modulation of cerebral hemodynamic function and improvement of stroke outcome. We investigated the hypothesis that in vivo 17beta-estradiol treatment of ovariectomized rats increases cerebrovascular prostacyclin production via elevation of the enzymes responsible for prostacyclin synthesis. METHODS: Cerebral blood vessels from 17beta-estradiol-treated and nontreated ovariectomized rats were isolated and examined for prostacyclin synthesis by enzyme-linked immunosorbent assay or for protein levels of cyclooxygenase-1, prostacyclin-synthase, and cytosolic phospholipase A2 by immunoblot analysis. RESULTS: We report that chronic in vivo 17beta-estradiol treatment significantly enhanced basal prostacyclin synthesis in rat cerebral blood vessels by 2.6-fold over control. 17beta-estradiol treatment also resulted in a 5.1-fold increase of cyclooxygenase-1 protein and a 6.7-fold increase of prostacyclin-synthase protein in the cerebral vasculature. There was no effect of estrogen on levels of cytosolic phospholipase A2. CONCLUSIONS: Our findings suggest that estrogen influences the biosynthesis of prostacyclin, which may be important in the regulation of cerebral blood flow and thrombosis. This finding may shed light on the mechanisms that govern sex-based differences in cerebrovascular disease.
BACKGROUND AND PURPOSE: It has been reported that estrogens modulate peripheral vascular synthesis of vasodilatory hormones, including prostacyclin. If this occurs in the cerebral circulation, it could have important consequences in the modulation of cerebral hemodynamic function and improvement of stroke outcome. We investigated the hypothesis that in vivo 17beta-estradiol treatment of ovariectomized rats increases cerebrovascular prostacyclin production via elevation of the enzymes responsible for prostacyclin synthesis. METHODS: Cerebral blood vessels from 17beta-estradiol-treated and nontreated ovariectomized rats were isolated and examined for prostacyclin synthesis by enzyme-linked immunosorbent assay or for protein levels of cyclooxygenase-1, prostacyclin-synthase, and cytosolic phospholipase A2 by immunoblot analysis. RESULTS: We report that chronic in vivo 17beta-estradiol treatment significantly enhanced basal prostacyclin synthesis in rat cerebral blood vessels by 2.6-fold over control. 17beta-estradiol treatment also resulted in a 5.1-fold increase of cyclooxygenase-1 protein and a 6.7-fold increase of prostacyclin-synthase protein in the cerebral vasculature. There was no effect of estrogen on levels of cytosolic phospholipase A2. CONCLUSIONS: Our findings suggest that estrogen influences the biosynthesis of prostacyclin, which may be important in the regulation of cerebral blood flow and thrombosis. This finding may shed light on the mechanisms that govern sex-based differences in cerebrovascular disease.
Authors: Emily J Su; Linda Ernst; Nadine Abdallah; Robert Chatterton; Hong Xin; Diana Monsivais; John Coon; Serdar E Bulun Journal: J Clin Endocrinol Metab Date: 2011-08-10 Impact factor: 5.958
Authors: Patricia Coutinho; Christopher Vega; Luminita H Pojoga; Alicia Rivera; Gregory N Prado; Tham M Yao; Gail Adler; Manuel Torres-Grajales; Enrique R Maldonado; Arelys Ramos-Rivera; Jonathan S Williams; Gordon Williams; Jose R Romero Journal: Endocrinology Date: 2014-03-21 Impact factor: 4.736
Authors: Whitney Wharton; Carey E Gleason; Katelin R Lorenze; Tamara S Markgraf; Michele L Ries; Cynthia M Carlsson; Sanjay Asthana Journal: Am J Transl Res Date: 2009-01-20 Impact factor: 4.060