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 Ca ²⁺-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 M] 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 Ca ²⁺-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.