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Am J Physiol Heart Circ Physiol (May 16, 2002). doi:10.1152/ajpheart.00934.2001
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Articles in PresS, published online ahead of print May 16, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00934.2001
Submitted on October 30, 2001
Accepted on May 8, 2002

Differential distribution of Kir2.1 and 2.3 subunits in canine atrium and ventricle

Peter Melnyk1, Liming Zhang2, Alvin Shrier3, and Stanley Nattel4*

1 Pathology, McGill University, Montreal, Quebec, Canada; Medicine, Research Center, Montreal Heart Institute, Montreal, Quebec, Canada
2 Medicine, Research Center, Montreal Heart Institute, Montreal, Quebec, Canada
3 Physiology, McGill University, Montreal, Quebec, Canada
4 Medicine, Research Center, Montreal Heart Institute, Montreal, Quebec, Canada; Medicine, University of Montreal, Montreal, Quebec, Canada; Pharmacology, McGill University, Montreal, Quebec, Canada

* To whom correspondence should be addressed. E-mail: nattel{at}icm.umontreal.ca.

Ventricular inward-rectifier current (IK1) is substantially larger than atrial, producing functionally important action potential differences. To evaluate possible molecular mechanisms, we recorded IK1 with patch-clamp and studied Kir2.1 and 2.3 subunit expression. IK1 density was >10-fold larger in canine ventricle than atrium. Kir2.1 protein expression (Western blot) was 78% greater(P < 0.01) in ventricle, but Kir2.3 band density was 228% greater (P < 0.01) in atrium. Immunocytochemistry showed transverse-tubular localization of Kir2.1 in 89% (17/19) of ventricular and 26% (5/19, P < 0.0001) of atrial cells. Both exhibited a weakly-positive Kir2.1 signal at the intercalated disks. Kir2.3 was strongly-expressed at the intercalated disks in all cells and in the transverse-tubular regions in 78% (14/18) of atrial and 22% (4/18, P < 0.001) of ventricular cells. Tissue immunohistochemical results qualitatively resembled isolated cell data. We conclude that the expression density and subcellular localization of Kir2.1 and 2.3 subunits differ in canine atrium versus ventricle. Overall protein density differences are insufficient to explain IK1 discrepancies, which may be related to differences in subcellular distribution.




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