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Pulmonary vasodilatory action of testosterone: evidence of a calcium antagonistic action

Richard D Jones1, Kate M English, Peter J Pugh

  • 1Academic Unit of Endocrinology, Division of Genomic Medicine, The University of Sheffield, UK. R.D.Jones@sheffield.ac.uk

Journal of Cardiovascular Pharmacology
|May 22, 2002
PubMed

Insights

Testosterone dilates pulmonary arteries by blocking calcium channels, independent of androgen receptors or nitric oxide. This finding reveals a new mechanism for testosterone

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Pulmonary Circulation

Background:

  • Testosterone benefits the cardiovascular system, acting as a coronary vasodilator.
  • Testosterone reduces myocardial ischemia in men with coronary heart disease.

Purpose of the Study:

  • To investigate testosterone's vasodilatory action in the pulmonary circulation.
  • To elucidate the mechanism underlying testosterone-induced pulmonary vasodilation.

Main Methods:

  • Pulmonary arteries from male rats were isolated and mounted in a wire myograph.
  • Vessels were preconstricted, and the vasodilatory effect of testosterone was measured.
  • The role of nitric oxide, prostaglandins, androgen receptors, and calcium channels was assessed.

Main Results:

  • Testosterone induced significant pulmonary artery dilation.
  • This dilation was independent of nitric oxide (l-NAME), prostaglandins (indomethacin), or androgen receptors (flutamide).
  • Testosterone's action was primarily against voltage-gated calcium channels, not calcium-independent pathways.

Conclusions:

  • Testosterone induces pulmonary vasodilation through a novel mechanism.
  • This mechanism involves calcium channel antagonism, independent of classic androgen pathways.
  • Testosterone's vasodilatory effect in the pulmonary circulation offers new therapeutic insights.

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