Properties and pharmacological modification of ATP‐sensitive K+ channels in cat tracheal myocytes

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Abstract
The effects of levcromakalim and nucleoside diphosphates (NDPs) on both membrane currents and unitary currents in cat trachea myocytes were investigated by use of patch‐clamp techniques. In conventional whole‐cell configuration, levcromakalim produced a concentration‐dependent K+ current which was suppressed by additional application of 5 μM glibenclamide at −70 mV. When 3 mM ATP was added in the pipette solution, the peak amplitude of the levcromakalim‐induced current was much smaller than that in the absence of ATP. When 3 mM uridine 5′‐diphosphate (UDP) was included in the pipette solution, much higher concentrations of glibenclamide (50 μM) were required to suppress the 100 μM levcromakalim‐induced membrane current in comparison with those in the absence of UDP. In the cell‐attached patches, levcromakalim activated a 40 pS K+ channel which was inhibited by additional application of glibenclamide in symmetrical 140 mM K+ conditions. UDP (0.1 mM) was capable of reactivating the channel in inside‐out patches in which the glibenclamide‐sensitive K+ channel had run down, in the presence of levcromakalim. The K+ channel reactivated by UDP was suppressed by additional application of either intracellular 3 mM ATP or 100 μM glibenclamide. These results demonstrate that smooth muscle cells in the cat trachea possess ATP‐sensitive 40 pS K+ channels which are blocked by glibenclamide (i.e. KATP) and can be activated by levcromakalim and that intracellular UDP causes a significant shift of the glibenclamide‐sensitivity of these channels. British Journal of Pharmacology (2000) 130, 625–635; doi:10.1038/sj.bjp.0703333

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