La testosterona inhibe las respuestas contráctiles del agonista adrenérgico α1, fenilefrina, asociadas con la liberación de calcio intracelular en la aorta de rata

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[10-5-10-4m]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 gq-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.