K<sub>ATP</sub>Channels in the Cardiovascular System

  • Monique N. Foster
    Departments of Pediatrics, Physiology & Neuroscience, and Biochemistry and Molecular Pharmacology, NYU School of Medicine, New York, New York
  • William A. Coetzee
    Departments of Pediatrics, Physiology & Neuroscience, and Biochemistry and Molecular Pharmacology, NYU School of Medicine, New York, New York

抄録

<jats:p>K<jats:sub>ATP</jats:sub>channels are integral to the functions of many cells and tissues. The use of electrophysiological methods has allowed for a detailed characterization of K<jats:sub>ATP</jats:sub>channels in terms of their biophysical properties, nucleotide sensitivities, and modification by pharmacological compounds. However, even though they were first described almost 25 years ago (Noma 1983, Trube and Hescheler 1984), the physiological and pathophysiological roles of these channels, and their regulation by complex biological systems, are only now emerging for many tissues. Even in tissues where their roles have been best defined, there are still many unanswered questions. This review aims to summarize the properties, molecular composition, and pharmacology of K<jats:sub>ATP</jats:sub>channels in various cardiovascular components (atria, specialized conduction system, ventricles, smooth muscle, endothelium, and mitochondria). We will summarize the lessons learned from available genetic mouse models and address the known roles of K<jats:sub>ATP</jats:sub>channels in cardiovascular pathologies and how genetic variation in K<jats:sub>ATP</jats:sub>channel genes contribute to human disease.</jats:p>

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