Journal of Pharmacological Sciences | |
Endoplasmic Reticulum Is a Key Organella in Bradykinin-Triggered ATP Release From Cultured Smooth Muscle Cells | |
Takeshi Katsuragi2  Takahiro Iwamoto2  Sadaharu Usune1  Yumei Zhao2  Chiemi Sato2  Keisuke Migita3  | |
[1] Research Laboratory of Biodynamics, School of Medicine, Fukuoka University, Japan;Department of Pharmacology, School of Medicine, Fukuoka University, Japan;Rehabilitation Medicine, Institute Brain Science, Hirosaki University School of Medicine, Japan | |
关键词: bradykinin B2 receptor; extracellular ATP release; inositol 1; 4; 5-trisphosphate [Ins(1; 4; 5)P3]-mediated Ca2+ signaling; endoplasmic reticulum; cultured smooth muscle cell; | |
DOI : 10.1254/jphs.FP0070865 | |
学科分类:药学 | |
来源: Nihon Yakuri Gakkai Henshuubu / Japanese Pharmacological Society | |
【 摘 要 】
References(37)Cited-By(10)ATP has broad functions as an autocrine/paracrine molecule. The mode of ATP release and its intracellular source, however, are little understood. Here we show that bradykinin via B2-receptor stimulation induces the extracellular release of ATP via the inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]-signaling pathway in cultured taenia coli smooth muscle cells. It was found that bradykinin also increased the production of Ins(1,4,5)P3 and 2-APB-inhibitable [Ca2+]i. The evoked release of ATP was suppressed by the Ca2+-channel blockers, nifedipine, and verapamil. Moreover, the extracellular release of ATP was elicited by photoliberation of Ins(1,4,5)P3. Bradykinin caused a quick and transient accumulation of intracellular ATP from cells treated with 1% perchloric acid solution (PCA), but not with the cell lysis buffer. Peak accumulation was prevented by 2-APB and thapsigargin, but not by nifedipine or verapamil, inhibitors of extracellular release of ATP. These findings suggest that bradykinin elicits the extracellular release of ATP that is mediated by the Ins(1,4,5)P3-induced Ca2+ signaling and, finally, leads to a Ca2+-dependent export of ATP from the cells. Furthermore, the bradykinin-induced transient accumulation of ATP in the cells treated with PCA may imply a possible release of ATP from the endoplasmic reticulum.
【 授权许可】
Unknown
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