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(Hypertension. 2001;38:1003.)
© 2001 American Heart Association, Inc.

Scientific Contributions

Acute Gender-Specific Hemodynamic and Inotropic Effects of 17ß-Estradiol on Rats

Martin E. Beyer; Georg Yu; Hartmut Hanke; Hans Martin Hoffmeister

From the Medizinische Klinik, Abt III, Eberhard-Karls-Universität (M.E.B., G.Y., H.M.H.), Tübingen, Germany; and Medizinische Klinik, Abt II, Universität Ulm (H.H.), Ulm, Germany.

Correspondence to Priv-Doz Dr Martin E. Beyer, Medizinische Universitätsklinik, Abt III, Otfried-Müller-Str 10, 72076 Tübingen, Germany. E-mail martin.beyer{at}med.uni-tuebingen.de

Abstract—— Estrogen has cardioprotective effects. In addition to beneficial effects on lipid metabolism, estrogen affects the vascular tone and may reduce endothelial dysfunction. In the present study, we examined acute gender-specific hemodynamic and inotropic effects of 17ß-estradiol (17ß-E) versus the control situation in open-chest rats. In addition to measurements in the intact circulation, myocardial function was examined on the basis of isovolumic registration independent of peripheral vascular effects. Regarding the dose-dependent and gender-specific effects of 17ß-E, in female rats, 17ß-E (50, 100, or 200 ng/kg) increased cardiac output (CO) (26%, 43%, and 59% versus control animals) as a result of reduction in total peripheral resistance (TPR) (-13%, -18%, and -24%) without any effect on myocardial contractility (isovolumic left ventricular systolic pressure, -1%, 0%, and -6%). These vascular effects are less pronounced in male rats (for 200 ng/kg 17ß-E: CO, 34%; TPR, -14%). We investigated gender-specific effects of 200 ng/kg 17ß-E after pretreatment with the estrogen receptor (ER) antagonist ICI 182,780. ER blockade reduced the effects of estrogen in female rats (CO, 29%; TPR, -17%) and male rats (CO, 19%; TPR, -11%). Regarding the effects of 200 ng/kg 17ß-E after pretreatment with N^G-nitro-L-arginine methyl ester, NO synthesis inhibition completely prevented the acute vascular effects of estrogen in female rats (CO, -4%; TPR, 1%). In addition, immunohistochemical staining revealed no gender-specific differences of the vascular ER distribution. 17ß-E caused an acute dose-dependent and gender-specific reduction in the afterload. ERs are involved in both genders in this vasodilative effect that is mediated by NO. This NO-mediated effect may explain in part the cardioprotective effect of estrogen.

Key Words: estrogen • receptors, estrogen • nitric oxide • hemodynamics • contractility • rats, Wistar

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