Resumen
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 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.
Título traducido de la contribución | Testosterone inhibits the contractile responses to α1- adrenergic agonist, phenylephrine, associated with the release of intracellular calcium in rat aorta |
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Idioma original | Español |
Páginas (desde-hasta) | 1-8 |
Número de páginas | 8 |
Publicación | Gaceta Medica de Mexico |
Volumen | 142 |
N.º | 1 |
Estado | Publicada - ene. 2006 |
Palabras clave
- Adrenergic agonists
- Intracellular Ca release
- Testosterone