Chronic intermittent hypoxia exposure reduces NOS isoforms in internal pudendal artery: linking sleep apnea and erectile dysfunction

Sleep apnea (SA) is characterized by chronic intermittent hypoxia (CIH) and is known to negatively impact vascular function. Erectile dysfunction (ED) is strongly associated with SA, which may result from vasculogenic complications of the internal pudendal artery, the vascular bed critical for erection formation. SA‐mediated alterations of the vasculature, including the contribution of nitric oxide synthase (NOS) isoforms, could promote ED. We hypothesize that CIH treatment will reduce NOS isoform proteins in the internal pudendal artery. Adult male rats were exposed to CIH (between 8am and 4pm, alternating 21% and 10% O2 every 3 min) or sham for 7 days. The internal pudendal artery was removed and western blot analysis was performed to determine protein levels for endothelial nitric oxide synthase (eNOS), neuronal NOS (nNOS) and inducible NOS (iNOS). Internal pudendal arteries from CIH treated rats had significantly reduced protein levels compared to sham for eNOS (0.5±0.03 vs 0.7±0.05), nNOS (0.4±0.03 vs 0.6±0.07) and iNOS (0.2±0.01 vs 0.3±0.02). These data suggest that CIH exposure reduces total NOS isoform protein levels in the internal pudendal artery, which may attenuate bioavailable NO necessary to achieve/maintain an erection. These results are the first to demonstrate that the SA‐mediated ED may be manifested through alterations in internal pudendal artery function.