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Am J Physiol Heart Circ Physiol (May 2, 2002). doi:10.1152/ajpheart.00515.2001
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Articles in PresS, published online ahead of print May 2, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00515.2001
Submitted on June 12, 2001
Accepted on April 24, 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, United Kingdom
2 Department of Occupational Diseases, National Institute of Industrial Health, Ministry of Labour, Kanagawa, Japan
3 Department of Neurochemistry, University of Tokyo, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: m.r.boyett{at}leeds.ac.uk.

The cardiac muscarinic K+ channel was studied in cultured neonatal rat atrial cells and in CHO cells transfected with receptor (hm2), channel (GIRK1 and GIRK4) and receptor kinase (GRK2). In atrial cells incubated in 10 µM carbachol (CCh) 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 (i) not transfected with the receptor kinase, (ii) transfected with a mutant receptor lacking phosphorylation sites (rather than the wild-type receptor) or (iii) 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.




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