Tamesue S, Sato C, Katsuragi T
Department of Pharmacology, School of Medicine, Fukuoka University, Japan.
Naunyn Schmiedebergs Arch Pharmacol. 1998 Mar;357(3):240-4. doi: 10.1007/pl00005163.
Histamine (60 microM) produced ATP release from segments of guinea-pig vas deferens which was blocked by pyrilamine and triprolidine, H1-blockers, but not by ranitidine, an H2-blocker. The evoked-release was inhibited by the mitochondrial inhibitors, carbonyl cyanide-m-chlorophenylhydrazone (CCCP) and oligomycin. Bradykinin (BK) and substance P (SP) also caused substantial and moderate release of ATP, respectively. The BK-evoked release of ATP was inhibited by HOE140, a B2-antagonist, but not by [Des-Arg10] HOE140, a B1-antagonist. On the other hand, VIP, angiotensin II (AII) and cholecystokinin-octapeptide (CCK-8) failed to elicit a measurable release of ATP. Histamine and BK also enhanced the release of ATP from superfused cultured smooth muscle cells. These results suggest that ATP may be released as an autacoid from the smooth muscles in the presence of these chemical mediators.
组胺（60微摩尔）可使豚鼠输精管段释放三磷酸腺苷（ATP），组胺H1受体阻滞剂吡苄明和曲普利啶可阻断这一过程，而H2受体阻滞剂雷尼替丁则无此作用。诱发性释放可被线粒体抑制剂羰基氰化物-间氯苯腙（CCCP）和寡霉素抑制。缓激肽（BK）和P物质（SP）也分别引起大量和中等程度的ATP释放。BK诱发的ATP释放可被B2拮抗剂HOE140抑制，但不能被B1拮抗剂[去精氨酸10]HOE140抑制。另一方面，血管活性肠肽（VIP）、血管紧张素II（AII）和八肽胆囊收缩素（CCK-8）未能引发可测量的ATP释放。组胺和BK还增强了超灌流培养平滑肌细胞中ATP的释放。这些结果表明，在这些化学介质存在的情况下，ATP可能作为一种自分泌物质从平滑肌中释放出来。
