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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Wong, T. M. Liu, J. Tsang, S. Wu, S. |
| Description | Author Affiliation: Tsang S ( Department of Physiology, LKS Faculty of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China.) |
| Abstract | BACKGROUND AND PURPOSE: Testosterone alleviates symptoms in patients with ischaemic heart disease. Androgen receptors are present in the heart, and testosterone upregulates gene expression of cardiac beta(1)-adrenoceptors. We hypothesize that testosterone may confer cardioprotection by interacting with adrenoceptors. EXPERIMENTAL APPROACH: In isolated perfused hearts and ventricular myocytes from orchidectomized rats without or with testosterone (200 microg/100 g) replacement, we first determined the effect of ischaemia/reperfusion in the presence of noradrenaline (10(-7) M). Then we determined the contribution of interactions between testosterone and alpha(1)- or beta(1)-adrenoceptors in cardiac injury/protection (infarct size, release of lactate dehydrogenase, viability of myocytes, recovery of contractile function and incidence of arrhythmias) upon ischaemia/reperfusion by pharmacological manipulation using selective adrenoceptor agonists (alpha(1)-adrenoceptor agonist: phenylephrine 10(-6) M; non-selective beta-adrenoceptor agonist: isoprenaline 10(-7) M) and antagonists (alpha(1): prazosin or benoxathian 10(-6) M; beta(1): CGP 20712A 5 x 10(-7) M). We also determined the expression of alpha(1) and beta(1)-adrenoceptor in the hearts from rats with and without testosterone. KEY RESULTS: Testosterone reduced injury induced by ischaemia/reperfusion and noradrenaline. This was achieved by enhancing the beneficial effect of alpha(1)-adrenoceptor stimulation, which was greater than the deleterious effect of beta(1)-adrenoceptor stimulation (also enhanced by testosterone). The effects of testosterone were abolished or attenuated by blockade of androgen receptors. Testosterone also enhanced the expression of alpha(1A) and beta(1)-adrenoceptor. CONCLUSIONS AND IMPLICATIONS: Testosterone conferred cardioprotection by upregulating the cardiac alpha(1)-adrenoceptor and enhancing the effects of stimulation of this adrenoceptor. The effect of testosterone was at least partly mediated by androgen receptors. |
| ISSN | 00071188 |
| e-ISSN | 14765381 |
| Journal | British Journal of Pharmacology |
| Issue Number | 4 |
| Volume Number | 153 |
| Language | English |
| Publisher | Wiley Online Library(on behalf of The British Pharmacological Society) |
| Publisher Date | 2008-02-01 |
| Publisher Place | Great Britain (UK) |
| Access Restriction | Open |
| Subject Keyword | Adrenergic Agonists Metabolism Myocytes, Cardiac Norepinephrine Orchiectomy Receptors, Adrenergic, Alpha-1 Receptors, Androgen Reperfusion Injury Prevention & Control Testosterone Administration & Dosage Adrenergic Antagonists Pharmacology Androgen Antagonists Animals Arrhythmias, Cardiac Cell Survival Cyproterone Acetate Disease Models, Animal L-Lactate Dehydrogenase Myocardial Contraction Myocardial Infarction Drug Effects Pathology Rats, Sprague-Dawley Receptor Cross-Talk Receptors, Adrenergic, Beta-1 Receptors, Adrenergic, Beta-2 Physiopathology Blood Time Factors Up-Regulation Ventricular Function, Left Research Support, Non-U.S. Gov't |
| Content Type | Text |
| Resource Type | Article |
| Subject | Pharmacology |
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