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Am J Physiol Heart Circ Physiol (January 24, 2002). doi:10.1152/ajpheart.00807.2001
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Articles in PresS, published online ahead of print January 24, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00807.2001
Submitted on September 13, 2001
Accepted on January 17, 2002

A 4-aminopyridine-sensitive current is enhanced by chronic carbon monoxide in coronary artery myocytes

Christine Barbe1, Eric Dubuis2, Annie Rochetaing3, Paul Kreher3, Pierre Bonnet2, and Christophe Vandier2*

1 U.F.R. Sciences, Unite de Preconditionnement du Myocarde, ANGERS, France; The Medical School, Department of Physiology, BIRMINGHAM, United Kingdom
2 Faculte de Medecine, Laboratoire de Physiopathologie de la Paroi Arterielle (LABPART), TOURS, France
3 U.F.R. Sciences, Unite de Preconditionnement du Myocarde, ANGERS, France

A physiological role of carbon monoxide has been suggested for coronary myocytes. However, direct evidence is lacking. The objective of the study was to test the effect of chronic carbon monoxide exposure on the K+ currents of the coronary myocytes. The effect of 3-week chronic exposure to carbon monoxide was assessed on K+ currents in isolated rat left coronary myocytes using the patch-clamp technique in the whole-cell configuration. Moreover, membrane potential studies were performed on coronary artery rings using intracellular microelectrodes and coronary blood flow in isolated heart preparation was recorded. Carbon monoxide did not change the amplitude of global whole-cell K+ current but it increased the component sensitive to 1 mM 4-aminopyridine. Carbon monoxide exposure hyperpolarized coronary artery segments by ~10 mV and therefore increased their sensitivity to 4-aminopyridine. This effect was associated with an enhancement of coronary blood flow. We conclude that chronic carbon monoxide increases a 4-aminopyridine-sensitive current in isolated coronary myocytes. This mechanism could in part contribute to the hyperpolarization and to the increase in coronary blood flow observed with carbon monoxide.




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