RETRACTED: CLONING AND FUNCTIONAL EXPRESSION OF A RAT-HEART K-ATP CHANNEL (RETRACTED ARTICLE. SEE VOL 378, PG 792, 1995)

POTASSIUM channels that are ATP-sensitive (K-ATP) couple membrane potential to the metabolic status of the cell. K-ATP channels are inhibited by intracellular ATP and are stimulated by intracellular nucleotide diphosphates(1). K-ATP channel are important regulators of secretory processes and muscle contraction, and are targets for therapeutic treatment of type II diabetes by the inhibitory sulphonylureas(2) and for hypertension by activators such as pinacidil(3). In cardiac tissue, K-ATP channels are central regulators of post-ischaemic cardioprotection(4,5). Electrophysiological and pharmacological characteristics vary among K-ATP channels recorded from diverse tissues suggesting extensive molecular heterogeneity(1) A complementary DNA encoding a K-ATP channel was isolated from rat heart using the polymerase chain reaction. We report here that the expressed channels possess all of the essential features of native cardiac K-ATP channels, including sensitivity to intracellular nucleotides. In addition the cloned channels are activated by the potassium channel opener, pinacidil, but are not inhibited by the sulphonylurea, glibenclamide.