Acute gender-specific hemodynamic and inotropic effects of 17 beta-estradiol on rats

Estrogen has cardioprotective effects. In addition to beneficial effects on lipid metabolism, estrogen affects the vascular tone and may reduce endoth elial dysfunction. In the present study, we examined acute gender-specific hemodynamic and inotropic effects of 17 beta -estradiol (17 beta -E) versus the control situation in open-chest rats. In addition to measurements in t he intact circulation, myocardial function was examined on the basis of iso volumic registration independent of peripheral vascular effects. Regarding the dose-dependent and gender-specific effects of 17 beta -E, in female rat s, 17 beta -E (50, 100, or 200 ng/kg) increased cardiac output (CO) (26%, 4 3%, and 59% versus control animals) as a result of reduction in total perip heral resistance (TPR) (-13%, -18%, and -24%) without any effect on myocard ial contractility (isovolumic left ventricular systolic pressure, -1%, 0%, and -6%). These vascular effects are less pronounced in male rats (for 200 ng/kg 17 beta -E: CO, 34%; TPR, -14%). We investigated gender-specific effe cts of 200 ng/kg 17 beta -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%). Regard ing the effects of 200 ng/kg 17,beta -E after pretreatment with N-G-nitro-L -arginine methyl ester, NO synthesis inhibition completely prevented the ac ute vascular effects of estrogen in female rats (CO, -4%; TPR, 1%). In addi tion, immunohistochemical staining revealed no gender-specific differences of the vascular ER distribution. 17 beta -E caused an acute dose-dependent and gender-specific reduction in the afterload. ERs are involved in both ge nders in this vasodilative effect that is mediated by NO. This NO-mediated effect may explain in part the cardioprotective effect of estrogen.