Sarcolemmal K(ATP) channels in the heart: molecular mechanisms brought to light, but physiologic consequences still in the dark.
ATP-sensitive potassium (K(ATP)) channels are inhibited by intracellular ATP and thus couple the metabolic state of the cell to its electrical activity. Tremendous progress has been made in the identification of the molecular basis of K(ATP) channel function and regulation. The answer to one key question, however, has proven elusive: What are the precise conditions for, and functional consequences of, sarcolemmal K(ATP) activation in physiologic and pathophysiologic states? Here we consider recent studies of the molecular basis of cardiac K(ATP) channel activity and the role of these channels in cardiac function during ischemia.
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Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA. cnichols@cellbio.wustl.edu
Nichols
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D000255:Adenosine Triphosphate / Q000032:analysis / Q000502:physiology*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology / Q000628:therapy; D004562:Electrocardiography; D006321:Heart / Q000502:physiology*; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D008958:Models, Molecular; D015221:Potassium Channels / Q000032:analysis / Q000502:physiology*; D012508:Sarcolemma / Q000737:chemistry*
D015221:Potassium Channels; D000255:Adenosine Triphosphate