| Research Abstract |
ATP is extracellularly released as an autocine/paracrine and served as a functional modulator via stimulating P2-receotors of cell types.
Hitherto, however, it remains unprovided evidence for the release mechanism and intracellular source of ATP. The research project was planed to clarify the existence of CaィイD12+ィエD1-signal pathway from endoplasmic reticulum (ER) to mitochondria in the release for ATP. In 1998, we demonstrated in ideal longitudinal smooth muscles of guinea-pigs that the release of ATP evoked by stimulating P2Y-purioceptors with α, β-methylene ATP (α, β-mATP) resulted from increase of Ins(1, 4, 5)PィイD23ィエD2 production via activation of phospholipase C and subsequently, from enhanced release of CaィイD12+ィエD1 from CaィイD12+ィエD1 storage sites. From the study during 1999 carried out with the vas deferens smooth muscles, it has been considered the possibility that α, β-mATP stimulates P2X-purinodeptors and, then activates ryanodine receptors on endoplasmic reticulum (ER), like caffeine, and the subsequent release of CaィイD12+ィエD1 from ER generating the release of ATP. The evoked release of ATP seen in both smooth muscles was interfered with mitochondrial inhibitors such as rotenone. Accordingly, it is suggested that release of ATP couples with CaィイD12+ィエD1-signal pathways from ER to mitochondria. The viewpoint will be clarified in a further analysis using fluorescent CaィイD12+ィエD1-probes to measure [CaィイD12+ィエD1]i in cultured rat hepatocytes without contractility.
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