AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 283: H819-H828, 2002. First published May 2, 2002; doi:10.1152/ajpheart.00515.2001
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Vol. 283, Issue 2, H819-H828, August 2002

Role of receptor kinase in long-term desensitization of the cardiac muscarinic receptor-K+ channel system

Z. Shui1, I. A. Khan1, H. Tsuga2, H. Dobrzynski1, T. Haga3, Z. Henderson1, and M. R. Boyett1

1 School of Biomedical Sciences, University of Leeds, Leeds LS2 9JT, United Kingdom; 2 Department of Occupational Diseases, National Institute of Industrial Health, Ministry of Labour, Kanagawa 214; and 3 Department of Neurochemistry, Faculty of Medicine, University of Tokyo, Tokyo 113-0033, Japan

Desensitization of the cardiac muscarinic K+ channel was studied in cultured neonatal rat atrial cells and in Chinese hamster ovary (CHO) cells transfected with muscarinic receptor (HM2), G protein-coupled inward rectifying K+ channels 1 and 4, and G protein-coupled receptor kinase 2. In atrial cells incubated in 10 µM carbachol for 24 h, channel activity in cell-attached patches was substantially reduced as a result of long-term desensitization. The long-term desensitization was also observed in CHO cells transfected with the wild-type receptor and receptor kinase (as well as the channel). However, long-term desensitization was greatly reduced or abolished if the cells were 1) not transfected with the receptor kinase, 2) transfected with a mutant receptor lacking phosphorylation sites (rather than the wild-type receptor), or 3) transfected with a mutant receptor kinase lacking kinase activity (rather than the wild-type receptor kinase). We suggest that long-term desensitization of the cardiac muscarinic receptor-K+ channel system to muscarinic agonist may involve phosphorylation of the receptor by receptor kinase.

heart; acetylcholine; potassium current


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