Received December 27, 2007
Revised February 6, 2008
Accepted after revision April 28, 2008

¹ Xuzhou Medical College

^* To whom correspondence should be addressed. E-mail: sunh{at}xzmc.edu.cn.

	Abstract

Abstract Women with functional ovaries have a lower cardiovascular risk than men and post-menopausal women. However, estrogen replacement therapy remains controversial. This study examined the effect of ovarian hormone deficiency and estrogen replacement on ventricular myocyte contractile function and -ARs expression. Sprague-Dawley female rats were subjected to bilateral ovariectomy (Ovx) or sham operation (Sham). A subgroup of Ovx rats received estrogen (E₂) replacement (40ug.kg^-1.day^-1) for 4 weeks. Cardiomyocytes shortening amplitude were evaluated including basal and isoprenaline (ISO) stimulation contraction. The expressions of -ARs were assessed by Western blotting. The release of lactate dehydrogenase(LDH) activity in the coronary effluent was determined with a LDH kit. Ovx promoted body weight gain associated with reduced serum E₂ and uterine weight, all of which were abolished by E₂. Ovx increased both basal and ISO stimulation contractions, increased LDH release, up-regulated 1-AR expression, down-regulated ₂-AR expression, all of which were restored by E₂. CGP20712A, a 1-AR antagonist, but not ICI118,551, a ₂-AR antagonist significantly decreased ventricular myocytes shortening amplitude. E₂ decreased cardiomyocytes contraction and expression of 1-AR, increased expression of ₂-AR, which was abolished by the E₂ receptor antagonist ICI182,780. These data suggest that estrogen plays a cardioprotective role in female rat ischemia/reperfusion injury hearts that is associated with decreased cardiomyocytes contraction and expression of ₁-AR, increased expression of ₂-AR. Key Words: Oestrogen; Ischemia; beta-adrenoreceptor

Key Words: Adrenoceptor, Ischaemia, Oestrogen