Testosterone and coronary vascular tone: implications in coronary artery disease.
The greater incidence of coronary artery disease in men compared to women has often suggested possible harmful effects of male sex steroids that could promote coronary atherogenesis and vasoconstriction. However, antiatherogenic and coronary vasodilator effects of testosterone have also been suggested. The interaction of testosterone (T) with its specific receptors may trigger not only long-term genomic effects, but also acute non-genomic vasodilator responses. Testosterone may activate the endothelium and stimulate the nitric oxide-cGMP and/or the hyperpolarization-mediated vascular relaxation pathway. T may also inhibit the signaling mechanisms of smooth muscle contraction such as [Ca2+]i and protein kinases. The T-induced stimulation of endothelium-dependent mechanisms of vascular relaxation and inhibition of the mechanisms of coronary smooth muscle contraction represent potential beneficial effects of T against coronary artery disease.
Research and Development, Department of Veterans Affairs Medical center, Harvard Medical School West Roxbury, Massachusetts 02132, USA.
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Wynne
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Khalil
D002118:Calcium / Q000378:metabolism; D003324:Coronary Artery Disease / Q000378:metabolism*; D006152:Cyclic GMP / Q000378:metabolism; D042783:Endothelial Cells / Q000378:metabolism; D005260:Female; D006801:Humans; D008074:Lipoproteins / Q000097:blood; D008297:Male; D009119:Muscle Contraction / Q000502:physiology; D009131:Muscle, Smooth, Vascular / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism; D011944:Receptors, Androgen / Q000378:metabolism; D013739:Testosterone / Q000378:metabolism*
D008074:Lipoproteins; D011944:Receptors, Androgen; D009569:Nitric Oxide; D013739:Testosterone; D006152:Cyclic GMP; D002118:Calcium