KCh channels are novel Ca2+-activated K+ channels responsible for the acetylcholine-evoked hyperpolarization in the endothelium of rat aorta.
Identifies KCh channels as novel calcium-activated potassium channels responsible for acetylcholine-evoked hyperpolarization in rat aortic endothelium.
Single K+ channel currents and membrane potential were recorded in the endothelium of excised intact rat aorta. 2. Two types of K+ channel were found in excised patches, KCh and KAp. With Na+ and K+ as the main external and internal cations, outward conductances were 6.7 pS (KCh) and 2.8 pS (KAp). In symmetric 150 mM K+, the inward conductances were 18 and 9.1 pS. 3. Activation by Ca2+ was concentration dependent. KCh channels were activated by Ca2+ > 0.1 microM and KAp by Ca2+ > 0.5 microM. 4. Apamin at concentrations > 1 nM inhibited KAp Channels. Block was complete at 10 nM. KAp channels were insensitive to charybdotoxin. KCh channels were inhibited by charybdotoxin at concentrations > 50 nM, but were insensitive to apamin. 5. d-Tubocurarine (dTC) evoked flickering activity of KAp channels at concentrations > 5 microM and complete block at 100 microM. At these doses, dTC did not affect KCh channels, but at concentrations > 1 mM it decreased the single channel amplitude. 6. Hyperpolarization evoked by acetylcholine was unaffected by apamin or dTC at low concentrations ( 50 nM) or dTC ( > 1 mM). 7. These data suggest that KCh channels are novel Ca(2+)-activated K+ channels responsible for the ACh-evoked hyperpolarization in the endothelium of rat aorta.
Марченко et al. (Mon,) reported a other. Apamin, charybdotoxin, d-Tubocurarine, acetylcholine was evaluated on K+ channel currents and membrane potential. KCh channels are novel Ca2+-activated K+ channels responsible for the acetylcholine-evoked hyperpolarization in the endothelium of rat aorta.