2006, Number 1
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Gac Med Mex 2006; 142 (1)
Testosterone inhibits the contractile responses to phenilephrine associated with the release of intracellular calcium in rat aorta.
Castillo C, Castillo EF, López J, López RM
Language: Spanish
References: 30
Page: 1-8
PDF size: 145.95 Kb.
ABSTRACT
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 Ca
2+ 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 Ca
2+-release channels) associated with capacitative Ca2
+ influx through non-L-type Ca
2+ 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 Ca
2+ influx through both L-type and non-L-type Ca
2+ 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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