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This Article Full Text Full Text (PDF) All Versions of this Article: 287/4/H1721    most recent 00224.2004v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in ISI Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (6) Citing Articles via Google Scholar Google Scholar Articles by Miyazaki, K. Articles by Dobson, J. G. Search for Related Content PubMed PubMed Citation Articles by Miyazaki, K. Articles by Dobson, J. G., Jr.

Protein kinase C and the antiadrenergic action of adenosine in rat ventricular myocytes

Department of Physiology, University of Massachusetts Medical School, Worcester, Massachusetts 01655

Submitted 8 March 2004 ; accepted in final form 4 June 2004

Adenosine-induced antiadrenergic effects in the heart are mediated by adenosine A₁ receptors (A₁R). The role of PKC in the antiadrenergic action of adenosine was explored with adult rat ventricular myocytes in which PKC was overexpressed. Myocytes were transfected with a pEGFP-N1 vector in the presence or absence of a PKC construct and compared with normal myocytes. The extent of myocyte shortening elicited by electrical stimulation of quiescent normal and transfected myocytes was recorded with video imaging. PKC was found localized primarily in transverse tubules. The A₁R agonist chlorocyclopentyladenosine (CCPA) at 1 µM rendered an enhanced localization of PKC in the t-tubular system. The -adrenergic agonist isoproterenol (Iso; 0.4 µM) elicited a 29–36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Iso-produced increase in shortening in all three groups, the reduction caused by CCPA was greatest with PKC overexpression. The CCPA reduction of the Iso-elicited shortening was eliminated in the presence of a PKC inhibitory peptide. These results suggest that the translocation of PKC to the t-tubular system plays an important role in A₁R-mediated antiadrenergic actions in the heart.

-adrenergic; cardiomyocyte shortening; transfection; t tubules; PKC translocation

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