Key result
Recent studies highlight the molecular basis of cardiac K(ATP) channel activity and their role in cardiac function during ischemia, though their precise physiologic consequences remain elusive.
This review highlights the molecular basis of cardiac K(ATP) channel activity and their role in cardiac function during ischemia.
K(ATP) channel roles in ischemia remain mechanistically unclear; hypothesis-generating for therapies but should not yet change practice.
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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Flagg et al. (2001) conducted a review in Cardiac ischemia. Sarcolemmal KATP Channels was evaluated. Recent studies highlight the molecular basis of cardiac K(ATP) channel activity and their role in cardiac function during ischemia, though their precise physiologic consequences remain elusive.
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