Artículos de revistas
Improvement In Relaxation Response In Corpus Cavernosum From Trained Rats.
Registro en:
Urology. v. 63, n. 5, p. 1004-8, 2004-May.
1527-9995
10.1016/j.urology.2003.11.034
15135008
Autor
Claudino, Mário A
Priviero, Fernanda B M
Teixeira, Cleber E
de Nucci, Gilberto
Antunes, Edson
Zanesco, Angelina
Institución
Resumen
To evaluate the contractile and relaxing responses in rat corpus cavernosum (RCC) from rats after 8 weeks of run training, because erectile function is highly dependent on nitric oxide (NO) from nitrergic fibers or endothelium. Physical activity enhances NO production and improves endothelial function, with beneficial effects on cardiovascular disease. The training program consisted of 8 weeks of run training, 5 days/wk, and each session lasted 60 minutes. The RCC was isolated, and concentration-response curves to NO, acetylcholine, sodium nitroprusside, phenylephrine, and endothelin were obtained. The excitatory and inhibitory effects of electrical field stimulation (2 to 32 Hz) were also evaluated. NO (0.1 to 100 microM) and sodium nitroprusside (0.01 to 1000 microM) produced a relaxing effect in RCC in a dose-dependent manner, with the maximal responses to NO (control 62% +/- 4%, trained 88% +/- 3%) and sodium nitroprusside (control 83% +/- 3%, trained 95% +/- 2%) significantly enhanced after 8 weeks of run training. However, acetylcholine-induced relaxations were not affected by exercise. Similarly, electrical field stimulation-induced relaxations were significantly increased in RCC from trained rats at 2 Hz (control 2.4% +/- 0.3%, trained 4.2% +/- 0.5%) and 4 Hz (control 5.3% +/- 1.2%, trained 12.5% +/- 1.7%). The contractile sensitivity of RCC to phenylephrine (0.01 to 100 microM) and endothelin (0.01 to 100 nM) was not modified by training exercise. Our findings suggest that run training enhances functional responses in rat RCC that involves increases in the NO-cyclic guanosine monophosphate signaling pathway by endothelium-independent mechanisms that is not accompanied by changes in contractile sensitivity. 63 1004-8