Background: We investigated, previously, the mechanism by which extracellular acidification promotes relaxation in rat thoracic aorta. These studies suggested that extracellular acidosis promotes vasodilation mediated by NO, KATP and SKCa, and maybe other K(+) channels in isolated rat thoracic aorta. This study was carried out to investigate the paxilline-mediated hyperpolarization induced by acid exposure.
Results: The relaxation response to HCl-induced extracellular acidification (7.4-6.5) was measured in rat aortic rings pre-contracted with phenylephrine (PE, 10(-6) M). The vascular reactivity experiments were performed in endothelium-intact and denuded rings, in the presence of paxilline (10(-6) M), which is an inhibitor of high calcium conductance potassium BKCa channels. In rings with endothelium, paxilline inhibits relaxation, triggered by acidification at all pH values lower than 7.2 and had no effect on rings without endothelium, showing that the activation of BKCa is endothelium-dependent.
Conclusion: High conductance potassium channel activation induced by acid exposure is endothelium-dependent.