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Am J Physiol Regul Integr Comp Physiol (February 6, 2003). doi:10.1152/ajpregu.00041.2003
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Submitted on January 24, 2003
Accepted on February 4, 2003

Improved erectile function following Rho-kinase inhibition in a rat castrate model of erectile dysfunction

Christopher J Wingard1*, John A Johnson2, Andre Holmes1, and Anita Prikosh1

1 Physiology, Medical College of Georgia, Augusta, GA, USA
2 Pharmacology and Toxicology, Medical College of Georgia, Augusta, GA, USA

* To whom correspondence should be addressed. E-mail: Cwingard{at}mail.mcg.edu.

Androgens are reported to act as strong modulators of erectile function influencing both nitric oxide and vasoconstrictor signaling. Castration results in a depressed erectile response that is associated with a loss of nitric oxide production and increased responsiveness to constrictive agents. The increased vasoconstrictor response may be a result of an active RhoA/Rho-kinase signaling pathway. We report here results of studies designed to test the hypothesis that inhibition of the Rho-kinase pathway restores erectile function in a castrate model by relaxing the smooth muscle. Mean arterial (MAP) and corpus cavernosal (CCP) pressures were monitored during intracavernosal injection of the Rho-kinase inhibitor Y-27632. Castration reduced the maximal erectile response (CCP/MAP) by 33 % and testosterone-replacement restored the response (Intact, 0.736 ± 0.040; Castrate, 0.492 ± 0.022; testosterone, 0.681 ± 0.073). Injection of Y-27632 increased CCP in all experimental groups it also left shifted the voltage response curve and increased the maximal CCP/MAP response (Intact, 0.753 ± 0.091; Castrate, 0.782 ± 0.081; Testosterone-treated, 0.894 ± 0.033). Y-27632 dose dependently relaxed phenylephrine stimulated cavernosal tissues. Cavernosal tissues showed increased RhoA and Rho-kinase protein levels following castration. Our data supports the hypothesis that an active Rho/Rho-kinase pathway contributes to the reduced erectile response following castration due to an up regulation of RhoA/ Rho-kinase protein levels and that inhibition of this pathway may serve as an effective treatment for erectile dysfunction.




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