Chronic Escitalopram Treatment Induces Erectile Dysfunction by Decreasing Nitric Oxide Bioavailability Mediated by Increased Nicotinamide Adenine Dinucleotide Phosphate Oxidase Activity and Reactive Oxygen Species Production

The inhibitory effects of escitalopram on erectile and vascular function were not accompanied by a change in endothelial nitric oxide synthase, neuronal nitric oxide synthase, inducible nitric oxide synthase expression, or endothelial nitric oxide synthase activity, suggesting that the inhibitory effect is caused by a decrease in nitric oxide bioavailability mediated by increased NADPH oxidase and reactive oxygen species production.