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Am J Physiol Heart Circ Physiol 285: H1641-H1649, 2003. First published June 19, 2003; doi:10.1152/ajpheart.00346.2003
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Molecular basis of species-specific expression of repolarizing K+ currents in the heart

Stephen Zicha,1,2 Isaac Moss,1 Bruce Allen,1 Andras Varro,3 Julius Papp,3 Robert Dumaine,4 Charles Antzelevich,4 and Stanley Nattel1,2

1Department of Medicine and Research Center, Montreal Heart Institute and University of Montreal, Montreal H1T 1C8; 2Department of Pharmacology and Therapeutics, McGill University, Montreal, Quebec, Canada H3G 1Y6; 3Department of Pharmacology and Pharmacotherapy, University of Szeged, H-6701, and Research Unit for Cardiovascular Pharmacology, Hungarian Academy of Sciences, Szeged H-6701, Hungary; and 4Masonic Medical Research Laboratories, Utica, New York 13501-1787

Submitted 26 January 2003 ; accepted in final form 16 June 2003

There are important species-specific differences in K+ current profiles and arrhythmia susceptibility, but interspecies comparisons of K+ channel subunit expression are lacking. We quantified voltage-gated K+ channel (Kv) subunit mRNA and protein in rabbits, guinea pigs, and humans. Kv1.4, Kv4.2, and Kv4.3 mRNA was present in rabbits but undetectable in guinea pigs. MinK mRNA concentration in guinea pigs was almost threefold greater versus humans and 20-fold versus rabbits. MinK protein expression in guinea pigs was almost twofold that in humans and sixfold that in rabbits. KvLQT1 mRNA concentration was greatest in humans, and protein expression in humans was increased by ~2- and ~7-fold compared with values in rabbits and guinea pigs, respectively. The ether-a-go-go-related gene (ERG1) mRNA was more concentrated in humans, but ERG1 protein expression could not be compared across species because of epitope sequence differences. We conclude that important interspecies differences in cardiac K+ channel subunit expression exist and may contribute to the following: 1) lack of a transient outward current in the guinea pig ({alpha}-subunit transcription absent in the guinea pig heart); 2) small slow delayed rectifier current and torsades de pointes susceptibility in the rabbit (low-level minK expression); and 3) large slow component of the delayed rectifier current in the guinea pig (strong minK expression).

arrhythmia; ion channels; electrophysiology; ECG; antiarrythmic drugs; proarrhythmia


Address for reprint requests and other correspondence: S. Nattel, Montreal Heart Institute, Research Center, 5000 Belanger St. E., Montreal, Quebec, Canada H1T 1C8 (E-mail: nattel{at}icm.umontreal.ca).




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