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Andrologia ; 54(8): e14477, 2022 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-35596534

RESUMO

The exact mechanism by which testosterone deficiency causes ED has not yet been elucidated. TRPC is involved in the process of smooth muscle cell contraction and relaxation. The effect of androgens on TRPCs and their relationship with erectile function are currently unclear. Thirty male SD rats were randomly divided into six groups: control group, castration group, castration + testosterone (T) group (cast + T), control + transfection group (control + trans), control + empty transfection group and castration + transfection group (cast + trans). The transfection group rats were given with lentivirus (1 × 108 TU/mL, 15 µl) carrying the siRNA targeting TRPC4 gene in the rat penile cavernous tissue at 4 weeks after castration. The tests were performed at 5 weeks after castration. Comparing the cast group with the control, the ICPmax/MAP, p-eNOS/eNOS and NO levels in the rat penile tissue were significantly lower (p < 0.01) and the level of TRPC3, TRPC4 and TRPC6 in the rat penile tissue was significantly increased (p < 0.01). When the cast + trans group was compared to the cast group, ICPmax/MAP was markedly higher (p < 0.05), and the level of the TRPC4 was remarkably lower (p < 0.05). Low androgen levels might inhibit an erectile function through up-regulation of the expression of TRPC3, TRPC4 and TRPC6 in rat penile cavernous tissue. Inhibition the level of TRPC4 in rat penile tissue may improve the erectile function in low androgen levels.


Assuntos
Disfunção Erétil , Canais de Potencial de Receptor Transitório , Androgênios/farmacologia , Animais , Humanos , Masculino , Ereção Peniana , Pênis , Ratos , Ratos Sprague-Dawley , Canal de Cátion TRPC6/metabolismo , Testosterona/metabolismo , Canais de Potencial de Receptor Transitório/metabolismo , Canais de Potencial de Receptor Transitório/farmacologia
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