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CARDIOVASCULAR
1-Adrenoceptor upon Ischemic Insult in the Rat Heart
Department of Physiology, The University of Hong Kong, Hong Kong Special Administrative Region, China
To test the hypothesis that estrogen confers cardioprotection by suppressing the expression of 
-adrenoceptor (-AR), we first correlated the infarct size in response to ischemic insult and -AR stimulation with the expression of 1-AR in sham, ovariectomized (Ovx) and estrogen replaced (Ovx + E2) rats. When -AR is being activated during ischemia, the infarct size was significantly greater in Ovx than in the sham and Ovx + E2 rats. There is a negative correlation between the infarct size and the expression level of 1-AR as revealed by Western blotting and supported by binding analysis. Incubation of ventricular myocytes from Ovx rats with estrogen at 10-9 M for 24 and 48 h, but not 12 h, significantly reduced lactate dehydrogenase release when the myocytes are subjected to simulated ischemia. The cardioprotective effect of 24 h estrogen incubation was accompanied by a reduction in the protein expression level of 1-AR, which is estrogen receptor-dependent, whereas the lack of protection of 12-h estrogen incubation was not accompanied by any alterations in the expression level of 1–AR. Together, the result from present study suggested that it is most likely that the cardioprotective effect of long-term estrogen replacement is due to suppressing the enhanced expression of cardiac 1-AR in the Ovx rats, which in turn reduces cardiac injury when -AR is activated by sympathetic hyperactivity during ischemia. Therefore, suppression of the enhanced expression of cardiac 1-AR in Ovx rats represents a novel cardioprotective mechanism of estrogen replacement therapy.
Address correspondence to: Prof. T. M. Wong, Department of Physiology, Faculty of Medicine, The University of Hong Kong Special Administrative Region, China. E-mail: wongtakm{at}hkucc.hku.hk
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