Abstract

Recent studies have identified the existence of outward, depolarizing chloride currents in isolated rat, rabbit, and human corpus cavernosum muscle cells. However, few articles have demonstrated the functional role of chloride channels in vivo in corpus cavernosum smooth muscle. Aim. To investigate the role of calcium-dependent chloride channels in erectile function of rat corpus cavernosum smooth muscle. Adult male Wistar rats were used to perform an in vivo study in a rat model of erection. Both crura of the rats were isolated to in order to record intracavernosal pressure (ICP) during basal conditions and electrical stimulation of erection, with and without intracorporeal injection of norepinephrine, chloride transport inhibitors, and chloride channel blockers. ICP. ICP increased as the amplitude of electrical stimulation increased, and decreased in a dose-dependent manner (during electrical stimulation) as norepinephrine injection strength increased. Injection into the corpus cavernosum of the Cl(-) channel blockers, niflumic acid, anthracene-9-carboxylic acid, and 4,4'-diisothiocyano-2,2'-stilbene-disulfonic acid increased ICP. Injection into the corpus cavernosum of the Cl(-) channel transport inhibitors bumetanide, ethacrynic acid, and HCO(3)-free 4-(2-hydroxyethyl )-1-1- piperazine ethanesulphonic acid buffer, and also increase the ICP. The effects of both Cl(-) channel blockers and Cl(-) channel transport inhibitors on ICP were concentration-dependent. Our findings suggest that chloride channels play an important role in the regulation of corpus cavernous smooth muscle tone in vivo.

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