Adenosine triphosphate (ATP)-sensitive K+ (KATP) channels were discovered in the heart almost 30 years ago. They are present in multiple tissues and link membrane excitability to the metabolic state of the cell. Under physiological conditions, cardiac K ATP channels are predominantly closed, but they may open during exertion, stress, and ischemia. Experimental and modeling studies have shown that activation of sarcolemmal KATP channels causes dramatic action potential shortening in vitro, which can be cardioprotective. Conversely, there is emerging evidence that KATP channel mutations are linked to heart diseases, including congestive heart failure and arrhythmias. The debate regarding the role, and even the very existence, of mitochondrial KATP channels is still ongoing. Filling these knowledge gaps will require further study, and integration of results from basic cellular electrophysiology, to animal models and clinical disease. This chapter will address the current understanding of cardiac KATP channels regarding molecular composition, regulation of channel activity, and physiological and pathophysiological roles.

Original languageEnglish
Title of host publicationElectrical Diseases of the Heart
Subtitle of host publicationVolume 1: Basic Foundations and Primary Electrical Diseases
PublisherSpringer-Verlag London Ltd
Number of pages21
ISBN (Electronic)9781447148814
ISBN (Print)9781447148807
StatePublished - Jan 1 2013


  • ATP
  • Ischemia
  • Kir6.1
  • Kir6.2
  • Metabolism
  • Potassium channel
  • SUR1
  • SUR2A
  • Sulfonylurea receptor


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