In:
Arteriosclerosis, Thrombosis, and Vascular Biology, Ovid Technologies (Wolters Kluwer Health), Vol. 18, No. 6 ( 1998-06), p. 961-967
Abstract:
Abstract —The low prevalence of coronary heart disease in premenopausal women and its increase after menopause are well established. Although estrogen is thought to play a role in protecting the vasculature, the mechanism has not been fully clarified. The contribution of platelets to atherosclerotic cardiovascular diseases is well recognized. The present study focused on the still-controversial effect of estrogen on platelet function. We investigated the in vitro effects of estrogen on human platelets, including their aggregation, Ca 2+ metabolism, the synthesis of cyclic nucleotides, and NO (nitrite/nitrate) synthesis after stimulation with thrombin or ADP. Pretreatment of platelets with 17β-estradiol reduced the platelet aggregation induced by thrombin or ADP, whereas 17α-estradiol had no effect. 17β-Estradiol accelerated the recovery of [Ca 2+ ] i after the agonist-induced peak and reduced the area under the curve of accumulated platelet [Ca 2+ ] i but did not alter the baseline [Ca 2+ ] i , Ca 2+ influx induced by thrombin or ADP, the release of Ca 2+ from internal stores, or the size of internal Ca 2+ stores. Pretreatment of platelets with 17β-estradiol had no effect on the intracellular concentration of cAMP but increased that of cGMP in agonist-stimulated platelets. Additionally, 17β-estradiol increased the platelet concentration of nitrite/nitrate in a dose-dependent manner. These effects of 17β-estradiol on platelet aggregation, Ca 2+ metabolism, and NO synthesis were abolished by exposure to N G -monomethyl- l -arginine, an NO synthesis inhibitor. These results suggest that 17β-estradiol plays an important role in inhibiting platelet aggregation by promoting Ca 2+ extrusion or reuptake activity that is dependent on the production of cGMP by increasing NO synthesis.
Type of Medium:
Online Resource
ISSN:
1079-5642
,
1524-4636
DOI:
10.1161/01.ATV.18.6.961
Language:
English
Publisher:
Ovid Technologies (Wolters Kluwer Health)
Publication Date:
1998
detail.hit.zdb_id:
1494427-3
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