Journal
VASCULAR HEALTH AND RISK MANAGEMENT
Volume 4, Issue 6, Pages 1459-1466Publisher
DOVE MEDICAL PRESS LTD
DOI: 10.2147/VHRM.S3995
Keywords
human; pulmonary circulation; pulmonary hypertension; sex hormone; testosterone; vasodilation
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Funding
- Heart Research UK
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Aim: To assess for the fi rst time the vasodilatory effect of testosterone in the human pulmonary circulation utilizing both isolated human pulmonary arteries and isolated perfused human lungs. In addition, a secondary aim was to determine whether there was any difference in the response to testosterone dependant upon gender. Methods: Isolated human pulmonary arteries were studied by wire myography. Vessels were preconstricted with U46619 (1 nM-1 mu M) prior to exposing them to either testosterone (1 nM-100 mu M) or ethanol vehicle (< 0.1%). Isolated lungs were studied in a ventilated and perfused model. They were exposed to KCl (100 mM), prior to the addition of either testosterone (1 nM-100 mu M) or ethanol vehicle (< 0.1%). Results: Testosterone caused signifi cant vasodilatation in all preparations, but a greater response to testosterone was observed in the isolated perfused lungs, 24.9 +/- 2.2% at the 100 mu M dose of testosterone in the isolated pulmonary arteries compared to 100 +/- 13.6% at the 100 mu M dose in the isolated perfused lungs. No signifi cant differences in the response to testosterone were observed between sexes. Conclusion: Testosterone is an effi cacious vasodilator in the human pulmonary vasculature and this is not modulated by patient sex. This vasodilator action suggests that testosterone therapy may be benefi cial to male patients with pulmonary arterial hypertension.
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