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This Article Full Text Full Text (PDF) All Versions of this Article: 291/5/H2371    most recent 01145.2005v1 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 (1) Citing Articles via Google Scholar Google Scholar Articles by Campos, L. A. Articles by Baltatu, O. C. Search for Related Content PubMed PubMed Citation Articles by Campos, L. A. Articles by Baltatu, O. C.

Enhanced isoproterenol-induced cardiac hypertrophy in transgenic rats with low brain angiotensinogen

¹Institute of Research and Development, University of Paraiba Valley, Sao Jose dos Campos, Brazil; ²Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany; ³Department of Physiology, University of Mississippi Medical Center, Jackson, Mississippi; and ⁴Laboratory of Hypertension, Department of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, Brazil

Submitted 31 October 2005 ; accepted in final form 19 May 2006

We have previously shown that a permanent deficiency in the brain renin-angiotensin system (RAS) may increase the sensitivity of the baroreflex control of heart rate. In this study we aimed at studying the involvement of the brain RAS in the cardiac reactivity to the -adrenoceptor (-AR) agonist isoproterenol (Iso). Transgenic rats with low brain angiotensinogen (TGR) were used. In isolated hearts, Iso induced a significantly greater increase in left ventricular (LV) pressure and maximal contraction (+dP/dt_max) in the TGR than in the Sprague-Dawley (SD) rats. LV hypertrophy induced by Iso treatment was significantly higher in TGR than in SD rats (in g LV wt/100 g body wt, 0.28 ± 0.004 vs. 0.24 ± 0.004, respectively). The greater LV hypertrophy in TGR rats was associated with more pronounced downregulation of -AR and upregulation of LV -AR kinase-1 mRNA levels compared with those in SD rats. The decrease in the heart rate (HR) induced by the -AR antagonist metoprolol in conscious rats was significantly attenuated in TGR compared with SD rats (–9.9 ± 1.7% vs. –18.1 ± 1.5%), whereas the effect of parasympathetic blockade by atropine on HR was similar in both strains. These results indicate that TGR are more sensitive to -AR agonist-induced cardiac inotropic response and hypertrophy, possibly due to chronically low sympathetic outflow directed to the heart.

autonomic nervous system; sympathetic nervous system; -adrenoreceptor

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