Skip Navigation

Cardiovascular Research 1995 30(4):602-610; doi:10.1016/S0008-6363(95)00091-7
© 1995 by European Society of Cardiology
This Article
Right arrow Full Text (PDF)
Right arrow Erratum (v30,p1044)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Novotny, J.
Right arrow Articles by Ransnäs, L. A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Novotny, J.
Right arrow Articles by Ransnäs, L. A.
Related Collections
Right arrowRelated Article
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 1995, European Society of Cardiology

Alterations in G-protein-regulated transmembrane signalling induced in murine myocardium by coxsackievirus B3 infection

Jiri Novotnya, Petr Kvapila, Frantisek Jelinekb and Lennart A. Ransnäs*

aWallenberg Laboratory for Cardiovascular Research, Gothenburg University, S-41345 Gothenburg, Sweden
bDepartment of Pathology, School of Medicine, Charles University, 12844 Prague, Czech Republic

* Corresponding author.

Objective: Cardiomyopathy is usually associated with marked alterations in myocardial transmembrane signalling. Although acute viral myocarditis may result in chronic cardiomyopathy in some cases, the possible consequences of viral infection on function of the myocardial signal-transducing complex have not been explored. Therefore, the present study was designed to investigated the G-protein-regulated adenylyl cyclase signalling system in murine myocardium during myocarditis induced by coxsackievirus B3 (CVB3) infection. Methods: We examined the functional characteristics of adenylyl cyclase as well as the function and distribution of β-adrenoceptors, m-cholinoceptors and G-proteins in myocardial plasma membranes isolated from the hearts of mice with acute (7 days pi) or late phase (21 days pi) myocarditis and the obtained results were compared with the corresponding data determined in age-matched controls. Results: While the basal adenylyl cyclase activity was not significantly altered, the ability of forskolin, sodium fluoride and GTP{gamma}S to activate adenylyl cyclase was lowered by about 20% in samples from virus-infected animals. The level of Gs{alpha} in myocardial plasma membranes as well as the functional activity of Gs{alpha} was not affected by viral infection, but the Gi{alpha} content was increased by about 20%. The total number of β-adrenoceptors in myocardial plasma membranes increased by about 12–15% due to higher content of the β2-adrenoceptor subtype. Although the agonist-binding parameters of β-adrenoceptors were not significantly altered, the ability of these receptors to mediate stimulation of adenylate cyclase was markedly diminished (by 56–80%). The total number of m-cholinoceptors in samples derived from virus-infected mice increased considerably (by 29–59%) and a significant proportion of the receptors shifted to a higher affinity status, but their ability to transduce agonist signals was impaired. Conclusions: These data are the first to demonstrate that several different sites of the myocardial G-protein-regulated adenylyl cyclase signalling complex are significantly altered in acute as well as in late phase of CVB3-induced myocarditis.

KEYWORDS Signal transduction; G-proteins; Myocarditis; Coxsackievirus; Heart failure


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?

Related Article

Alterations in G-protein-regulated transmembrane signalling induced in murine myocardium by coxsackievirus B3 infection
Jiri Novotny, Petr Kvapil, Frantisek Jelinek, and Lennart A. Ransnäs
Cardiovasc Res 1995 30: 1044. [PDF]





Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.