Research of Ionic Channel and Its Intracellular Signalling Pathwa.

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(1) Ca^<2+>-activated Cl^- current in tracheal smooth msucle cells (TSMCs) : We recently reported that neurokinin A causes rapid and sustained depolarization of single TSMCs by two different mechanisms ; (1) initial transient activation of Ca^<2+>-dependent Ca^- current (ICa.L), and (2) sustained inhibition of K^+ currents (Pflugers Arch 1995, in press). The activation of Cl^- current was due to the release of Ca^<2+> from the IP_3-store sites. In addition, we further investigated that the underlying mechanisms of activation of Ca^<2+>-activated Cl^- current in single TSMCs, and found that ICa.L as well as agonist stimulation plays an important role in activating the current, where CICR-sensitive Ca^<2+>-store sites may be involved. Also, it is likely that in guinea -pig TSMCs, IP3 and CICR-sensitive Ca^<2+> store sites may be overlapping.(2) Mechanism of vasopressin and endothelin-induced calcium influx in aortic smooth msucle cells : The effects of vasopressin and endothelin on cultured rat aortic smooth muscle cells were investigated using the calcium-sensitive dye Indo-1 to measure intracellular Ca^<2+> and the patch clamp-technique. We found that calcium entry elicited by these agents is mediated by the receptoroperated Ca^<2+>-permeable non-selective cation channel in aortic smooth muscle cells (Heart and Vessels, 1995, in press). Also, the present results indicate that endothelin activates Ca^<2+>-dependent K^+ current (IK.Ca) and nonselective cation channel (IN.S.) via the ET_A receptor, and the activation of IK.Ca ismediated presumably by IP_3 and Ca^<2+> from internal store sites, but different mechanisms may be involved in activation of IN.S.via the pertussistoxin insensitive GTP-binding proteins (Circulation (abstract) 1994 : 90 : 200).