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Cardiovascular Research 1999 43(1):17-19; doi:10.1016/S0008-6363(99)00126-1
© 1999 by European Society of Cardiology
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Copyright © 1999, European Society of Cardiology

A new, sympathetic look at KATP channels in the heart

Carol Ann Remmea,* and Arthur A.M Wildea,b

aDepartment of Clinical and Experimental Cardiology, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands
bDepartment of Clinical Electrophysiology, Heart–Lung Institute, University Hospital, Utrecht, The Netherlands

* Corresponding author. Tel.: +31-20-566-3265; fax: +31-20-697-5458 c.a.remme@amc.uva.nl

Received 25 March 1999; accepted 25 March 1999

KEYWORDS Norepinephrine; Release; Myocardium; K-ATP channel; Ischaemia

The first 10% of the full text of this article appears below.

See article by Oe et al. ([10], pages 125–134) in this issue.


   1 Introduction
 
Myocardial ATP-sensitive potassium (KATP) channels are closed during physiological conditions but are activated by a decrease in intracellular ATP-concentration [1]. KATP activation during myocardial ischaemia postpones the onset of irreversible damage, and reduces the size of the area of myocardial infarction (reviewed in [2]). Blockade of KATP channels by sulfonylurea derivatives and sodium 5-hydroxydecanoate (5-HD) reverses these cardioprotective effects [2]. The exact mechanism of cardioprotection by KATP activation has not yet been unravelled. Shortening of action potential duration due to the opening of KATP channels [4,5], the previously supposed underlying mechanism, is not a prerequisite for cardioprotection to occur [3]. Mitochondrial KATP channels may . . . [Full Text of this Article]


   2 Catecholamine release, uptake and metabolism in the normal heart
 

   3 Catecholamine release during myocardial ischaemia/infarction
 

   4 Modulation of catecholamine release from the ischaemic myocardium
 

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