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This Article Full Text Full Text (PDF) All Versions of this Article: 93/9/1034    most recent expphysiol.2007.041939v3 expphysiol.2007.041939v2 expphysiol.2007.041939v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Google Scholar Articles by Wu, Q. Articles by Gu, S.-l. PubMed PubMed Citation Articles by Wu, Q. Articles by Gu, S.-l. Related Collections Cardiovascular control

Departments of ¹ Physiology² Pharmacology, Xuzhou Medical College, Xuzhou, Jiangsu 221002, China

Women with functional ovaries have a lower cardiovascular risk than men and postmenopausal women. However, oestrogen replacement therapy remains controversial. This study examined the effect of ovarian hormone deficiency and oestrogen replacement on ventricular myocyte contractile function and expression of β-adrenoceptors (β-ARs). Female Sprague–Dawley rats were subjected to bilateral ovariectomy (OVX) or sham operation (Sham). A subgroup of OVX rats received oestrogen (E₂) replacement (40 µg kg^–1 day^–1) for 4 weeks. Cardiomyocyte shortening was evaluated in basal conditions and in the presence of isoprenaline (ISO). The expression of β-ARs was assessed by Western blotting. The presence of lactate dehydrogenase (LDH) activity in the coronary effluent was determined. Ovariectomy promoted body weight gain associated with reduced serum E₂ and uterine weight, all of which were abolished by treatment with E₂. Ovariectomy increased the amplitude of both basal and ISO-stimulated contractions, increased LDH release, upregulated β₁-AR expression and downregulated β₂-AR expression, all of which were restored by treatment with E₂. A β₁-AR antagonist, CGP20712A, but not a β₂-AR antagonist, ICI118,551, significantly decreased the amplitude of ventricular myocyte shortening. Oestrogen decreased cardiomyocyte contraction and the expression of β₁-AR, and increased expression of β₂-AR, and all these effects were abolished by the E₂ receptor antagonist, ICI182,780. These data suggest that oestrogen plays a cardioprotective role in female rat hearts subjected to ischaemia–reperfusion injury, and the effects of oestrogen are associated with decreased cardiomyocyte contraction and expression of β₁-AR, and increased expression of β₂-AR.

(Received 27 December 2007; accepted after revision 28 April 2008; first published online 30 May 2008)
Corresponding author Hong Sun: West Huaihai Road 84, Xuzhou, Jiangsu 221002, China. Email: sunh{at}xzmc.edu.cn, hhwuq{at}yahoo.com.cn