Participation of calcium, released from the IP3-sensitive Ca-store in activation of Ca-dependent potassium conductance of ileal smooth muscle cells.

The apamin-, charybdotoxin- (CTX) and glibenclamide- (GLB) sensitive components, which form the active part of the net potassium outward current (IK) in single smooth muscle cells from the longitudinal layer of guinea-pig ileum (LC), were investigated for their sensitivity to calcium. The experiments were carried out by the whole-cell voltage-clamp method. A successful block of all Ca-sources (with heparin and nifedipine; heparin and cyclopiazonic acid while the intracellular Ca-concentration--[Ca2+]i--was kept at 3 x 10(-8) mol/l by 11 mmol/l EGTA into the pipette solution) led to the complete inhibition of IK. The deeply located Ca-sensitive Ca-pool was effectively isolated by the high concentration of the chelator, which was proved by the fact that ruthenium red and ryanodine failed to affect IK. The GLB-sensitive component of IK demonstrated Ca-gated properties, while both the other components were activated most probably by calcium, released form the IP3-sensitive Ca-pool. It was concluded that the IP3-induced Ca-release mechanism plays an important role in the regulation of K(+)-conductivity in LC.