Shinozuka K, Kunitomo M, Shimoura K, Hattori K
Department of Pharmacology, Faculty of Pharmaceutical Science, Mukogawa Women's University, Nishinomiya, Japan.
Jpn J Pharmacol. 1995 May;68(1):125-7. doi: 10.1254/jjp.68.125.
Potassium (40 mM) evoked the release of adenine nucleotides and adenosine in rat isolated caudal arteries. This release was abolished by bunazosin. Endogenous noradrenaline was also released. Furthermore, the high potassium-induced purine release was abolished by rubbing the lumen of the vessel. These findings suggest that the high potassium releases endogenous noradrenaline, which subsequently elicits the release of ATP and related purines by acting on alpha 1-adrenoceptors on the endothelial cell.
钾离子(40毫摩尔)可引起大鼠离体尾动脉中腺嘌呤核苷酸和腺苷的释放。布那唑嗪可消除这种释放。内源性去甲肾上腺素也会释放。此外,通过摩擦血管内腔可消除高钾诱导的嘌呤释放。这些发现表明,高钾释放内源性去甲肾上腺素,后者随后通过作用于内皮细胞上的α1肾上腺素能受体引发ATP及相关嘌呤的释放。