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Cardiac morphofunctional characteristics of transgenic rats with overexpression of the bradykinin B1 receptor in the endothelium
R. F. Levy, A. J. Serra, E. L. Antonio, L. Dos Santos, D. S. Bocalini, J. B. Pesquero, M. Bader, V. F. Merino, H. A. de Oliveira, E. C. de Arruda Veiga, J. A. Silva, P. J. Tucci
Language English Country Czech Republic
Document type Journal Article
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- MeSH
- Ventricular Dysfunction, Left genetics metabolism physiopathology MeSH
- Endothelial Cells metabolism MeSH
- Phenotype MeSH
- Ventricular Function, Left * MeSH
- Genetic Predisposition to Disease MeSH
- Myocardial Contraction * MeSH
- Papillary Muscles metabolism physiopathology MeSH
- Rats, Sprague-Dawley MeSH
- Rats, Transgenic MeSH
- Receptor, Bradykinin B1 genetics metabolism MeSH
- Ventricular Remodeling MeSH
- Up-Regulation MeSH
- Animals MeSH
- Check Tag
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
Our aim was to evaluate whether endothelial overexpressing of the bradykinin B1 receptor could be associated with altered left ventricular and myocardial performance. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function in Sprague Dawley transgenic rats overexpressing the endothelial bradykinin B1 receptor (Tie2B1 rats). The myocardial inotropism was evaluated on papillary muscles contracting in vitro. In Tie2B1 animals, an enlarged left ventricular cavity and lower fractional shortening coupled with a lower rate of pressure change values indicated depressed left ventricular performance. Papillary muscle mechanics revealed that both Tie2B1 and wild-type rat groups had the same contractile capacities under basal conditions; however, in transgenic animals, there was accentuated inotropism due to post-pause potentiation. Following treatment with the Arg(9)-BK agonist, Tie2B1 papillary muscles displayed a reduction in myocardial inotropism. Endothelial B1 receptor overexpression has expanded the LV cavity and worsened its function. There was an exacerbated response of papillary muscle in vitro to a prolonged resting pause, and the use of a B1 receptor agonist impairs myocardial inotropism.
Johns Hopkins University School of Medicine Baltimore USA
Max Delbrück Center for Molecular Medicine Berlin Buch Germany
Universidade Federal da Paraíba João Pessoa Paraíba Brazil
Universidade Federal de São Paulo São Paulo SP Brazil
Universidade Federal do Espírito Santo Vitória Espírito Santo Brazil
References provided by Crossref.org
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- $a Our aim was to evaluate whether endothelial overexpressing of the bradykinin B1 receptor could be associated with altered left ventricular and myocardial performance. Echocardiography and hemodynamic were employed to assess left ventricular morphology and function in Sprague Dawley transgenic rats overexpressing the endothelial bradykinin B1 receptor (Tie2B1 rats). The myocardial inotropism was evaluated on papillary muscles contracting in vitro. In Tie2B1 animals, an enlarged left ventricular cavity and lower fractional shortening coupled with a lower rate of pressure change values indicated depressed left ventricular performance. Papillary muscle mechanics revealed that both Tie2B1 and wild-type rat groups had the same contractile capacities under basal conditions; however, in transgenic animals, there was accentuated inotropism due to post-pause potentiation. Following treatment with the Arg(9)-BK agonist, Tie2B1 papillary muscles displayed a reduction in myocardial inotropism. Endothelial B1 receptor overexpression has expanded the LV cavity and worsened its function. There was an exacerbated response of papillary muscle in vitro to a prolonged resting pause, and the use of a B1 receptor agonist impairs myocardial inotropism.
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