Participation of calcium ion in ATP release from the vascular endothelial cells.

ATP释放机制的药理学研究：在大鼠尾动脉中，去甲肾上腺素（NA）引起ATP及其代谢物的显著释放，并被哌唑嗪、游离Ca^<2+>和摩擦内皮所消除。钠钾交换液增加了ATP的释放。而40mm KC1溶液和高渗溶液则降低了ATP的释放。因此，去极化可能促进ATP的释放。据报道，高渗透压会阻碍间隙连接的功能。l -庚醇，间隙连接抑制剂，消除ATP的释放。这表明atp的释放机制与Ca^<2+>内流和间隙结以电压依赖的方式密切相关。atp释放机制的显微镜研究：在大鼠尾动脉中，NA明显升高内皮细胞和平滑肌细胞内Ca^<2+>水平。另一方面，在培养的大鼠尾动脉内皮细胞中，NA并没有提高细胞内Ca^<2+>水平。此外，NA没有引起培养细胞中ATP的释放。这表明在内皮细胞和平滑肌细胞中，na诱发的atp释放与Ca^<2+>动员密切相关。ATP与一氧化氮作用机制的研究：在大鼠尾动脉中，缓激素（BK）产生内皮依赖性和l - name敏感性松弛，但不引起ATP的释放。BK明显提高尾动脉内皮细胞和平滑肌细胞内Ca^<2+>水平。此外，在培养细胞中，BK明显提高细胞内Ca^<2+>水平，但没有引起ATP的释放。这些结果表明，在内皮细胞中，BK诱导的no释放与Ca^<2+>动员密切相关，并且BK受体不与atp释放机制偶联。从目前的结果来看，atp释放与α _1-肾上腺素受体偶联和no释放与bk受体偶联的机制之间可能没有联系，尽管这两种释放都与Ca^<2+>密切相关。作为一种可能性，我们认为平滑肌细胞内Ca^<2+>的动员可能参与了内皮细胞释放ATP和平滑肌间隙连接，内皮细胞可能在其中起重要作用。少

Pharmacological studies on the mechanism of ATP-release :In the the rat caudal arteries, noradrenaline (NA) evoked a significant release of ATP and its metabolites, which was abolished by prazosin, Ca^<2+> free and rubbing of endothelium. The release of ATP was increased by the sodium-potassium exchange solution. But, 40 mM KC1 solution and hypertonic solution reduced the release of ATP.Therefore, depolarization may facilitate the release of ATP.It is reported that the function of gap junction is prevented by hyperosmolarity. L-heptanol, gap junction inhibitor, abolished the release of ATP.These suggest that the mechanisms of ATP-release is closely associated with Ca^<2+> influx and gap junction in voltage depent manner.Microscopic studies on the mechanism of ATP-release :In the rat caudal arteries, NA clearly raised intracellular Ca^<2+> levels in the endothelial and smooth muscle cells. On the other hand, in the cultured endothelial cells isolated from the rat caudal artery, NA did n … More ot raise intracellular Ca^<2+> level. Also, NA did not evoke the release of ATP in the cultured cells.These suggest that NA-evoked ATP-release is closely associated with Ca^<2+> mobilization in both endothelial and smooth muscle cells.Studies on the mechanisms of ATP and Nitric oxide :In the rat caudal arteries, bradykinin (BK) produced endothelium-dependent and L-NAME-sensitive relaxation, but did not evoke the release of ATP.BK clearly raised intracellular Ca^<2+> levels in the endothelial and smooth muscle cells of the caudal artery. Also, in the cultured cells, BK clearly raised intracellular Ca^<2+> levels, but did not evoke the release of ATP.These results suggest BK-evoked NO-release is closely associated with Ca^<2+> mobilization in endothelial cells alone and BK receptor does not couple with the mechanisms of ATP-release.From the present results, there may be no linkage between the mechanisms of ATP-release coupled with alpha_1-adrenoceptor and NO-release coupled with BK-receptor, although both releases are closely associated with Ca^<2+>. As one possibility, it is suggested that intracellular Ca^<2+> mobilization in smooth muscle cells may be involved in the release of ATP from endothelial cells and gap junctionbetween smooth muscle, and endothelial cells may play an important roles. Less