SUMMARY1. Properties of the pinacidil-sensitive K+ channel in the smooth muscle of the rabbit portal vein were investigated using cell-attached and inside-and outside-out patch clamp techniques.2. In the cell-attached patch configuration, a K+ channel with a unitary conductance of 150 pS could be recorded when physiological salt solution (PSS) was in the pipette and high-K+ solution was in the bath. Tetraethylammonium (TEA; < 1 mM) and charybdotoxin (CTX; > 50 nM) inhibited the 150 pS K+ channel from the outside of the membrane. This channel was activated by an increase in the concentrations of intracellular Ca2+ but not by pinacidil (< 500 gM).3. In the cell-attached patch configuration, bath application of pinacidil (> 3 jm) activated a K+ channel (ATP-sensitive K+ channel) with a unitary conductance of 15 pS and the enhancing action of pinacidil was blocked by glibenclamide. However, in the cell-free patch configuration, pinacidil (100 gM) failed to open the 15 pS K+ channel. With pinacidil in the pipette, the 15 pS K+ channel was completely inactivated within 5 s of the excision of the membrane. Opening of the 15 pS K+ channel also disappeared after saponin treatment (50 gug/ml).4. In the cell-free patch configuration, application of guanosine 5'-diphosphate (GDP; > 100 gM) re-activated the inactivated 15 pS K+ channel only when pinacidil was present either in the pipette or bath. GDP increased the mean open time and open probability of the 15 pS K+ channel in a concentration-dependent manner.

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A considerable body of evidence has revealed that interstitial cells of Cajal (ICC), identified with c-Kit-immunoreactivity, act as gut pacemaker cells, with spontaneous Ca2+ activity in ICC as the probable primary mechanism. Namely, intracellular (cytosolic) Ca2+ oscillations in ICC periodically activate plasmalemmal Ca2+-dependent ion channels and thereby generate pacemaker potentials. This review will, thus, focus on Ca2+-associated mechanisms in ICC in the gastrointestinal (GI) tract, including auxiliary organs.