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Physiological roles of ATP‐sensitive K + channels in smooth muscle
Author(s) -
Teramoto Noriyoshi
Publication year - 2006
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2006.105973
Subject(s) - sulfonylurea receptor , potassium channel , biophysics , myocyte , ion channel , intracellular , ligand gated ion channel , skeletal muscle , chemistry , vascular smooth muscle , cardiac action potential , membrane potential , biology , microbiology and biotechnology , biochemistry , receptor , electrophysiology , smooth muscle , neuroscience , anatomy , protein subunit , endocrinology , repolarization , gene
Potassium channels that are inhibited by intracellular ATP (ATP i ) were first identified in ventricular myocytes, and are referred to as ATP‐sensitive K + channels (i.e. K ATP channels). Subsequently, K + channels with similar characteristics have been demonstrated in many other tissues (pancreatic β‐cells, skeletal muscle, central neurones, smooth muscle). Approximately one decade ago, K ATP channels were cloned and were found to be composed of at least two subunits: an inwardly rectifying K + channel six family (Kir6.x) that forms the ion conducting pore and a modulatory sulphonylurea receptor (SUR) that accounts for several pharmacological properties. Various types of native K ATP channels have been identified in a number of visceral and vascular smooth muscles in single‐channel recordings. However, little attention has been paid to the molecular properties of the subunits in K ATP channels and it is important to determine the relative expression of K ATP channel components which give rise to native K ATP channels in smooth muscle. The aim of this review is to briefly discuss the current knowledge available for K ATP channels with the main interest in the molecular basis of native K ATP channels, and to discuss their possible linkage with physiological functions in smooth muscle.