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Cardiovascular Research 2006 72(2):220-230; doi:10.1016/j.cardiores.2006.07.011
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Copyright © 2006, European Society of Cardiology

Role of KATP channels in sepsis

James F. Buckleya,b, Mervyn Singerb and Lucie H. Clappa,*

aBritish Heart Foundation Laboratories and Bloomsbury Institute for Intensive Care Medicine, UK
bDepartment of Medicine, University College London, 5, University Street, London, WC1E 6JF, UK

* Corresponding author. BHF Laboratories, Department of Medicine, 4th Floor Rayne Building, University College, 5 University Street, London WC1E 6JF, UK. Tel.: +44 20 7679 6180; fax: +44 20 7679 6250. Email address: l.clapp{at}ucl.ac.uk

Sepsis is an infection-induced inflammatory syndrome responsible for ~10% of all deaths worldwide. While pathophysiological mechanisms remain to be fully unravelled, new insights and discoveries are yielding significant improvements in outcome, particularly in the high mortality conditions of shock and multi-organ failure. One potential target is the ATP-sensitive potassium (KATP) channel, an ion channel critical to the cardiovascular stress response. Excessive activation of the vascular channel is now recognised as a major cause of hypotension and vascular hyporesponsiveness to catecholamines in septic shock. Some researchers advocate therapeutic blockade of these channels; however, outside the vasculature, channel opening may actually represent a protective mechanism against cellular damage. In this review we critically examine the role of the KATP channel in sepsis.

KEYWORDS K-ATP channel; Sepsis; Septic shock; Vascular hyporeactivity; Multi-organ failure; Mitochondria; Insulin

Time for primary review 15 days


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