Endothelium-dependent relaxation in pudendal arteries is partially dependent upon nitroxyl anion

Erectile dysfunction (ED) has been shown to be associated with and even precede cardiovascular diseases (CVD) such as hypertension. Nitroxyl anion (HNO), a redox congener of nitric oxide (NO), has been demonstrated to be a potent vasodilator of both conduit and resistance vessels. Previous data from our laboratory suggests that HNO-mediated vasodilation exhibits a regional variability, as it was reduced during angiotensin II hypertension in mesenteric arteries as compared to aorta. There are currently no studies investigating the role of HNO as a possible mediator of erectile function. We hypothesize that HNO plays a role in erection by relaxing smooth muscle cells in the pudendal arteries (PA), which supplies blood flow to the penis, as well as in the corpus cavernosum (CC). CC and PA were isolated from Sprague-Dawley rats, and mounted on DMT myograph systems. Concentration response curves (CRC) to the HNO donor, Angeli's Salt (AS) and acetylcholine (ACh) were performed in phenylephrine-contracted, endothelium intact vessels and strips. CC strips did not exhibit a relaxation response to AS; in contrast, the PA exhibited an HNO-mediated relaxation response(EC50=-5.72±0.28). In addition, endothelium-mediated relaxation responses were attenuated when PA were incubated with the HNO scavenger, L-cysteine [3 mM] as compared to vehicle(Emax27.01%vs. 70.03%). These data suggest that, while the CC does not relax to HNO, the PA exhibits a relaxation response to HNO. Also, ACh-mediated relaxation was decreased using the HNO scavenger, suggesting that endothelium-mediated relaxation responses in the PA may partially be attributed to HNO as compared to NO.