Role of store-operated Ca2 entry in adenosine-induced vasodilatation of rat small mesenteric artery

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 vasodila-tion. This study was designed to examine the hypothesis that SOCE have a functional role in adenosine-induced vasodilation. Small mes-enteric 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 M) 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-mediate