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Published on: February 9, 2016
Testosterone and coronary vascular tone: implications in coronary artery disease
1Research and Development, Department of Veterans Affairs Medical center, Harvard Medical School West Roxbury, Massachusetts 02132, USA.
Insights
Testosterone may protect against coronary artery disease by promoting blood vessel relaxation and inhibiting smooth muscle contraction. These findings suggest beneficial cardiovascular effects of testosterone, challenging previous assumptions.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Vascular Biology
Background:
- Coronary artery disease (CAD) incidence is higher in men, implicating male sex steroids.
- Testosterone's role is debated, with suggestions of both harmful atherogenic/vasoconstrictive effects and beneficial antiatherogenic/vasodilator effects.
Purpose of the Study:
- To investigate the potential beneficial cardiovascular effects of testosterone.
- To explore the mechanisms by which testosterone may influence coronary artery function.
Main Methods:
- Examined the interaction of testosterone (T) with its specific receptors.
- Investigated both genomic and acute non-genomic effects of testosterone on vascular pathways.
- Assessed testosterone's impact on endothelial activation, nitric oxide-cGMP pathway, and hyperpolarization-mediated relaxation.
- Evaluated testosterone's inhibition of smooth muscle contraction signaling, including intracellular calcium ([Ca2+]i) and protein kinases.
Main Results:
- Testosterone interaction with receptors triggers genomic and acute non-genomic responses.
- Testosterone activates the endothelium, stimulating nitric oxide-cGMP and hyperpolarization-mediated vascular relaxation.
- Testosterone inhibits smooth muscle contraction signaling pathways.
Conclusions:
- Testosterone promotes endothelium-dependent vasodilation.
- Testosterone inhibits coronary smooth muscle contraction.
- These mechanisms suggest testosterone has beneficial effects against coronary artery disease.
Abstract:
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.
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