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Am J Physiol Heart Circ Physiol 282: H2031-H2038, 2002. First published January 24, 2002; doi:10.1152/ajpheart.00807.2001
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Vol. 282, Issue 6, H2031-H2038, June 2002

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

Christine Barbé1, Eric Dubuis2, Annie Rochetaing1, Paul Kreher1, Pierre Bonnet2, and Christophe Vandier2

1 Unité de Préconditionnement du Myocarde, Unité de Formation et de Recherche Sciences, 49045 Angers Cedex; and 2 Laboratoire de physiopathologie de la paroi artérielle, Faculté de Médecine, 37032 Tours, France

A physiological role of carbon monoxide has been suggested for coronary myocytes; however, direct evidence is lacking. The objective of this study was to test the effect of chronic carbon monoxide exposure on the K+ currents of the coronary myocytes. The effect of 3-wk chronic exposure to carbon monoxide was assessed on K+ currents in isolated rat left coronary myocytes by the use of 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 did increase 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 hyperpolarization and to increased coronary blood flow observed with carbon monoxide.

voltage-gated K+ channels; membrane currents; vasodilation; 4-aminopyridine


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