Abstract
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.
Original language | English |
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Article number | A261 |
Number of pages | 1 |
Journal | Hypertension |
Volume | 60 |
Issue number | S1 |
DOIs | |
Publication status | Published - 1 Sept 2012 |
Keywords
- nitroxyl anion (HNO)
- vasodilator agents
- arteries
- vasorelaxation
- pudendal arteries
- corpus cavernosum
- activation of potassium (K+) channels