Abstract
The purpose of this study was to investigate NADPH oxidase as a common mechanism underlying both erectile dysfunction (ED) and coronary artery disease (CAD) in inactivity and diet‐induced obesity. Male Sprague‐Dawley rats were fed a Western diet (WD) or Control diet (CD) for 12 weeks. Subgroups within each diet remained sedentary (Sed) or engaged in treadmill exercise (Ex) throughout the dietary intervention. Erectile function was evaluated by measuring the mean arterial pressure and intracavernosal pressure in response to electrical field stimulation of the cavernosal nerve, prior to and following an intracavernosal injection of apocynin (Apo; an NADPH oxidase inhibitor). Coronary artery endothelial function (CAEF) was evaluated ex vivo with cumulative doses of acetylcholine (ACh) applied to coronary artery segments pre‐constricted with serotonin. CAEF was assessed in the presence and absence of Apo. Erectile function (p < 0.0001) and CAEF (p < 0.001) were attenuated in WD‐Sed rats. Erectile function (p < 0.01) and CAEF (p < 0.05) were augmented by Apo only in WD‐Sed rats. Ex preserved erectile function (p < 0.0001) and CAEF (p < 0.05) within the WD. This study suggests that erectile function and CAEF are impaired by NADPH oxidase in chronic WD‐fed rats, while Ex training may be a practical means of preventing WD‐induced ED and CAD.Supported by the Sexual Medicine Society of North America.
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