Celotto Andrea Carla, Capellini Verena Kise, Albuquerque Agnes Afrodite Sumarelli, Ferreira Luciana Garros, Silveira Ana Paula Cassiano, de Nadai Tales Rubens, Evora Paulo Roberto Barbosa
Department of Surgery and Anatomy, Laboratory of Endothelial Function, School of Medicine, University of São Paulo, Av. Café, 3000, Ribeirão Preto, SP, Brazil.
, Av. Bandeirantes, 3900, HC-FMRP, 9o. andar, Ribeirão Preto, SP, 14.049-900, Brazil.
BMC Res Notes. 2015 Sep 19;8:462. doi: 10.1186/s13104-015-1422-3.
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.
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.
High conductance potassium channel activation induced by acid exposure is endothelium-dependent.
我们之前研究了细胞外酸化促进大鼠胸主动脉舒张的机制。这些研究表明,细胞外酸中毒促进由一氧化氮(NO)、ATP敏感性钾通道(KATP)和小电导钙激活钾通道(SKCa)以及分离的大鼠胸主动脉中其他可能的钾通道介导的血管舒张。本研究旨在探讨酸暴露诱导的哌克昔林介导的超极化作用。
在预先用去氧肾上腺素(PE,10⁻⁶ M)预收缩的大鼠主动脉环中测量对盐酸诱导的细胞外酸化(pH 7.4 - 6.5)的舒张反应。血管反应性实验在完整内皮和去内皮的血管环中进行,存在哌克昔林(10⁻⁶ M),其为高钙电导钾通道(BKCa)的抑制剂。在有内皮的血管环中,哌克昔林抑制在所有低于7.2的pH值下由酸化触发的舒张,并且对无内皮的血管环没有影响,表明BKCa的激活是内皮依赖性的。
酸暴露诱导的高电导钾通道激活是内皮依赖性的。