| Autor: |
Miyazaki, Koji, Komatsu, Satoshi, Ikebe, Mitsuo, Fenton, Richard A., Dobson Jr., James G. |
| Předmět: |
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| Zdroj: |
American Journal of Physiology: Heart & Circulatory Physiology; Oct2004, Vol. 287 Issue 4, pH1721-H1729, 9p, 12 Color Photographs, 10 Black and White Photographs, 1 Diagram, 8 Graphs |
| Abstrakt: |
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 tubule's. The A1R agonist chlorocyclopentyladenosine (CCPA) at 1 µM rendered an enhanced localization of PKC∈ in the t-tubular system. The β-adrenergic agonist isoproterenol (Iso; 0.4 µM) elicited a 29-36% increase in myocyte shortening in all three groups. Although CCPA significantly reduced the Isoproduced 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. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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