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Submitted on September 30, 2005
Accepted on March 1, 2006
Hormone and Vascular Biology Research Group, Academic Unit of Endocrinology, Division of Genomic Medicine, University of Sheffield, Sheffield S10 2RX; Department of Cardiology, Royal Hallamshire Hospital, Sheffield, S10 2JF; School of Medicine, University of Leeds, Leeds LS2 9JT; Barnsley Hospital NHS Foundation Trust, Barnsley, S75 2EP
* To whom correspondence should be addressed. E-mail: c.s.peers{at}leeds.ac.uk.
Testosterone has marked beneficial cardiovascular effects, many of which have been attributed to a vasodilatory action. However, the molecular target of testosterone underlying this effect is subject to debate. Here, we have used microfluorimetry as a non-invasive means of examining whether testosterone could exert dilatory effects via inhibition of voltage-gated Ca2+ entry in the model vascular smooth muscle cell line, A7r5. Rises of [Ca2+]i evoked by 50 mM K+-containing solution were suppressed in a concentration-dependent manner by testosterone (IC50 3.1 nM) and by the non-aromatizable analog, 5
-dihydrotestosterone (IC50 6.9 nM). The effects of testosterone were apparent in the presence of pimozide (to block T-type Ca2+ channels) but not nifedipine (to block L-type Ca2+ channels). Testosterone did not alter Ca2+ mobilization from intracellular stores by the prostaglandin analog U46619 or capacitative Ca2+ entry in cells pre-treated with thapsigargin. Our results indicate that testosterone, at physiological concentrations, can selectively suppress Ca2+ entry into A7r5 cells via L-type Ca2+ channels. We suggest this effect is a likely mechanism underlying its vasodilatory actions and beneficial cardiovascular effects.
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