ATP-sensitive potassium channels (K
ATP) are the ion channels which are closely associated with cellular metabolism. A number of chemical compounds which block K
ATP facilitate the release of hormones or neuropeptides. For example, K
ATP-blocking agents such as antidiabetic sulfonylureas and imidazolines stimulate insulin secretion from pancreatic β-cells by decreasing K
ATP activity. On the other hand, so-called potassium channel openers, K
ATP-activating drugs which constitute a chemically diverse group of compounds, inhibit growth hormone secretion from anterior pituitary cells and release of γ-aminobutylic acid from substantia nigra. Several endogenous substances also modulate release of hormone or neuropeptide by affecting K
ATP activity. Acetylcholine and histamine stimulate the release of endothelium-derived hyperpolarizing factor, which activates K
ATP in the plasma membrane of vascular smooth muscle cells. Both galanin and somatostatin inhibit insulin release from pancreatic β-cells by opening K
ATP through the activation of G-protein. Glucagon-like peptide-1 [7-36], which stimulates insulin secretion by indirectly blocking K
ATP in β-cells, shows antidiabetic effects in patients with non-insulin-dependent diabetes mellitus. Endosulphine, an endogenous inhibitor of K
ATP, stimulates insulin secretion from pancreatic β-cells. Accumulating knowledge of the modulation and function of K
ATP would help our understanding of the regulation and physiological role of hormones and neuropeptides.
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