Abstract
Men have a higher incidence of coronary heart disease than women at similar age until the age of 50. This finding has led to the hypothesis that testosterone may be a risk factor for coronary heart disease. However, the vascular actions of testosterone remain to be fully elucidated. The aim of this study was to investigate the relationship between testosterone and vascular reactivity, and the mechanism underlying this action. Changes in isometric tension were recorded in isolated rings of porcine coronary arteries. Rings, with disrupted endothelium, were incubated with testosterone in the absence or presence of various pharmacological inhibitors. Dose-response of the contraction agent, U46619 (a stable thromboxane A2 analogue), was then determined. Testosterone significantly enhanced contraction to U46619 in porcine coronary arteries. This effect of testosterone increased with increasing concentration, and was not affected by KT 5823 (a protein kinase G inhibitor). On the other hand, enhancement of U46619-induced contraction in porcine coronary arteries by testosterone was abolished by SQ 22536 (an adenylate cyclase inhibitor) or KT 5720 (a protein kinase A inhibitor). Our result suggested that the effect of testosterone on enhancement of contraction involved the cAMP pathway but not the cGMP pathway. This study was supported by a Committee on Research and Conference Grant from the University of Hong Kong.
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