Item Type: | Article |
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Title: | Reduced isoproterenol-induced renin-angiotensin changes and extracellular matrix deposition in hearts of TGR(A1-7)3292 rats |
Creators Name: | Nadu, A.P., Ferreira, A.J., Reudelhuber, T.L., Bader, M. and Santos, R.A. |
Abstract: | We investigated the expression of specific extracellular matrix (ECM) proteins in cardiac hypertrophy induced by isoproterenol in TGR(A1-7)3292 rats. Additionally, changes in circulating and tissue renin-angiotensin system (RAS) were analyzed. Left ventricles (LV) were used for quantification of collagen type I, III, and fibronectin using immunofluorescence-labeling techniques. Angiotensin (Ang) II levels were measured by radioimmunoassay. Expression of RAS components was assessed by semi-quantitative polymerase chain reaction (PCR) or real-time PCR. Isoproterenol treatment induced an increase in the expression of collagen I, III, and fibronectin in normal rats. Collagen I and fibronectin expression were decreased in TGR(A1-7)3292 at basal conditions and both proteins increased by isoproterenol treatment; however, the levels achieved were still significantly lower than those observed in treated normal rats. The increase in collagen III observed in normal rats was completely blunted in TGR(A1-7)3292. Moreover, TGR(A1-7)3292 presented lower Ang II levels and angiotensinogen expression and a higher angiotensin-converting enzyme 2 (ACE2) expression in LV. Isoproterenol treatment increased cardiac Ang II concentration only in normal rats, which was associated with an increase in ACE2 and a decrease in Mas expression. These observations suggest that Ang-(1-7) specifically modulates the expression of RAS components and ECM proteins in LV. |
Keywords: | Mas Receptor, ACE2, Collagen, Hypertrophy |
Source: | Journal of the American Society of Hypertension |
ISSN: | 1933-1711 |
Publisher: | Elsevier |
Volume: | 2 |
Number: | 5 |
Page Range: | 341-348 |
Date: | September 2008 |
Official Publication: | https://doi.org/10.1016/j.jash.2008.04.012 |
PubMed: | View item in PubMed |
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