Abstract

This study was designed to evaluate whether overconsumption of NaCl, a well-known risk factor for hypertension, leads to erectile dysfunction in rodents. Male Wistar rats received regular chow (control group) or 4% NaCl chow for 24 weeks and were subjected to blood pressure measurement and apomorphine-induced erection. Moreover, cavernosal strips from both the control and 4% NaCl groups were evaluated in organ baths. Animals subjected to 4% NaCl chow did not develop hypertension but presented a significant reduction in the total number of erections following apomorphine administration as compared with the control group. The addition of high KCl or phenylephrine resulted in similar contractile responses in the corpus cavernosal strips from both the control and 4% NaCl groups. However, electrical field stimulation-induced contraction was significantly enhanced in cavernosal strips from animals exposed to 4% NaCl. Incubation of Y-27632, but not of atropine and Nω-nitro-l-arginine methyl ester (L-NAME), entirely prevented the potentiation of the contractile responses evoked by electrical stimulation. The enhanced contractile responses evoked by electrical stimulation found in the high-salt group were also avoided in the absence of extracellular calcium. Concentration-response curves of CaCl2 revealed augmented contractility in response to extracellular calcium in cavernosal strips from the 4% NaCl-treated rats, compared with control samples. A high-salt diet alone rendered the animals less responsive to apomorphine-induced penile erection and enhanced neurally mediated contractile responses in the corpus cavernosum, a clear indication that overconsumption of sodium can lead to erectile dysfunction even without the development of hypertension.

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