Role of store-operated Ca2+ entry in adenosine-induced vasodilatation of rat small mesenteric artery
发布时间：2025-04-30
点击次数：
- 发布时间：
- 2025-04-30
- 论文名称：
- Role of store-operated Ca2+ entry in adenosine-induced vasodilatation of rat small mesenteric artery
- 发表刊物：
- Am J Physiol Heart Circ Physiol
- 摘要：
- Store-operated Ca2+ entry (SOCE) has recently been proposed to contribute to Ca2+ influx in vascular smooth muscle cells (VSMCs). Adenosine is known for its protective role against hypoxia and ischemia by increasing nutrient and oxygen supply through vasodilation. This study was designed to examine the hypothesis that SOCE have a functional role in adenosine-induced vasodilation. Small mesenteric resistance arteries and mesenteric VSMCs were obtained from rats. Isometric tensions of isolated artery rings were measured by a sensitive myograph system. Laser-scanning confocal microscopy was used to determine the intracellular Ca2+ concentration of fluo 3-loaded VSMCs. Adenosine (0.1–100 µM) relaxed artery rings that were precontracted by phenylephrine in a concentration-dependent manner. In cultured mesenteric VSMCs, passive store depletion by thapsigargin and active store depletion by phenylephrine both induced Ca2+ influx due to SOCE. Adenosine inhibited SOCE-mediated increases in cytosolic Ca2+ levels evoked by the emptying of the stores. In isolated artery rings, adenosine inhibited SOCE-induced contractions due to store depletion. A2A receptor antagonism with SCH-58261 and adenylate cyclase inhibition with SQ-22536 largely attenuated adenosine responses. The cAMP analog 8-bromo-cAMP mimicked the effects of adenosine on SOCE. Our results indicate a novel mechanism of vasodilatation by adenosine that involves regulation of SOCE through the cAMP signaling pathway due to activation of adenosine A2A receptors.
- 合写作者：
- Wang SP, Zang WJ*, et al
- 卷号：
- 297
- 页面范围：
- H347-H354
- 是否译文：
- 否
- 发表时间：
- 2009-04-29