Pinacidil opens the ATP-sensitive and Ca-dependent K channel in smooth muscle cells of the rat and rabbit portal veins

Two types of ATP‐sensitive potassium channels in rat portal vein smooth muscle cells

“…This could be a result of complex interactions between glibenclamide and KCO. Kajioka et al (1990) reported a small conductance K channel (10 pS with external K concentration of 6 mM) in rat portal vein smooth muscle cells which was activated by intracellular Ca and the KCO nicorandil and which was inhibited by 5 mM ATP. This small-conductance ATP-sensitive potassium channel has not been reported in other tissues and is apparently different from either the LK channel or the MK channel of the present experiments.…”

“…Zhang & T.B. Bolton ATP-sensitive potassium channels activity which underlies the whole cell currents described by others in rat portal vein smooth muscle cells (Kajioka et al, 1990; Noack et al, 1992a,b).…”

Potassium channel activation and relaxation by nicorandil in rat small mesenteric arteries

“…The properties of K ATP channels that have been reported to be activated by nicorandil and other K ATP channel openers in di erent smooth muscle tissues are quite diverse, however; in some cases the channels activated have been reported to show Ca 2+ -sensitivity (Kajioka et al, 1990). This may correspond to di erences in the isoforms of K ATP channel expressed (see Quayle et al, 1997 for review).…”

“…Clinically, in contrast to other nitrovasodilators, tolerance does not develop on continued application of nicorandil, and this lack of tolerance seems to be due its K + channel opening action (Frampton et al, 1992). K + current activation by nicorandil has been measured directly using patch clamp of smooth muscle cells cultured from porcine coronary artery (Miyoshi et al, 1992;Wakatsuki et al, 1992) and cells isolated from rat and rabbit portal vein (Kajioka et al, 1990;Kamouchi & Kitamura, 1994), but not so far in cells from small arteries. In both portal vein and coronary artery cells, nicorandil has been reported to activate channels that are inhibited by intracellular ATP (K ATP channels); in rat portal vein cells the channel activated by nicorandil has been reported to also be activated by intracellular Ca 2+ (Kajioka et al, 1990), while in rabbit portal vein cells the channel is activated by intracellular nucleoside diphosphates as well as inhibited by ATP (Kamouchi & Kitamura, 1994).…”

“…K + current activation by nicorandil has been measured directly using patch clamp of smooth muscle cells cultured from porcine coronary artery (Miyoshi et al, 1992;Wakatsuki et al, 1992) and cells isolated from rat and rabbit portal vein (Kajioka et al, 1990;Kamouchi & Kitamura, 1994), but not so far in cells from small arteries. In both portal vein and coronary artery cells, nicorandil has been reported to activate channels that are inhibited by intracellular ATP (K ATP channels); in rat portal vein cells the channel activated by nicorandil has been reported to also be activated by intracellular Ca 2+ (Kajioka et al, 1990), while in rabbit portal vein cells the channel is activated by intracellular nucleoside diphosphates as well as inhibited by ATP (Kamouchi & Kitamura, 1994). The sensitivity of nicorandil-activated currents in vascular smooth muscle to the sulphonylurea glibenclamide, which appears to be selective for K ATP channels in this tissue at concentrations up to 10 mM has not been investigated, though glibenclamide inhibition of nicorandilactivated currents has been reported in cells from the pig proximal urethra (Teramoto & Brading, 1997).…”