Abstract 261: Nitroxyl Anion Induced Vasorelaxation in Pudendal Arteries is Partially Mediated via the Large Conductance Calcium-activated Potassuim Channel
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 have demonstrated that the mechanism of HNO-mediated vasorelaxation varied according to the vascular bed. However, no studies address the role of HNO in erectile function. We have demonstrated that the corpus cavernosum does not exhibit a relaxation response to HNO. However, we have shown that the pudendal artery (PA), which supplies blood flow to the penis, does exhibit a relaxation response to HNO and that ACh-mediated relaxation responses may be partially attributed to HNO as compared to NO. We hypothesized that HNO mediates vasorelaxation in pudendal arteries via activation of potassium (K+) channels. PAs were isolated from Sprague-Dawley rats and concentration-response curves (CRC) to an HNO donor: Angeli’s Salt (AS) were performed in phenylephrine contracted vessels (1μM) in the absence and the presence of the calcium (Ca2+) -activated K+ channel inhibitors: TRAM-34 (intermediate Ca2+-activated K+-channel inhibitor, IKCa , 10 μM) , UCL-1689 (Small conductance calcium-activated potassium channel, SKCa ,1 μM), iberiotoxin (large conductance Ca2+-activated K+-channel inhibitor, BKCa ,0.1μM). There were no observed differences in relaxation responses to AS with IKCa and SKCa channel inhibition. In contrast, inhibition of BKCa channels resulted in a rightward shift in the CRC to AS (logEC50 -4.74±0.11 vs. -5.26±0.11, p<0.01) with no differences in Rmax. These data suggest that AS-dependent vasorelaxation in PA is partially mediated via BKCa channel activation.
- © 2012 by American Heart Association, Inc.