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Castillo C, Castillo EF, Lopez J, Lopez RM: [Testosterone inhibits the contractile responses to phenylephrine associated with the release of intracellular calcium in rat aorta]. Gac Med Mex. 2006 Jan-Feb;142(1):1-8. Using endothelium-denuded rat aortic rings incubated in Ca2+ -free solution, we assessed the ability of testosterone to influence the contractile effect of phenylephrine, and the increase in resting tone (IRT) associated with Ca2+ ability to cross the plasma membrane. The addition of testosterone [10 (-5)-10 (-4) 5 min before phenylephrine [10 (-6) M], inhibited both phenylephrine-induced contraction and IRT. These changes were not affected by cycloheximide (10 (-5) M; a protein synthesis inhibitor of), flutamide (10 (-5) M; an androgenic receptor antagonist), or by adding aminoglutethimide (10 (-5) M; an aromatase inhibitor). Testosterone also blocked the contractile response to serotonin [10 (-5) M] but not to caffeine [10 (-2) M]. On the other hand, testosterone inhibited the contractile responses to cyclopiazonic acid (10 (-6) M; a selective Ca2+ -ATPase inhibitor) or ryanodine (10 (-5 M; an activator of sarcoplasmic reticulum Ca2+ -release channels) associated with capacitative Ca2+ influx through non-L-type Ca2+ channels. These data suggest that by acting on the cellular membrane, testosterone interferes with the signal transduction pathway of G (q-11) protein-coupled receptors, and inhibits capacitative Ca2+ influx through both L-type and non-L-type Ca2+ channels. These effects are non-genomic, non-mediated by the intracellular androgen receptor, and not due to the conversion of testosterone to estrogens. |
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