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Am J Physiol Heart Circ Physiol 297: H1845-H1852, 2009. First published September 11, 2009; doi:10.1152/ajpheart.01135.2008
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Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism

Jörg Peters,1,2 Torsten Schlüter,1,2 Thomas Riegel,1,2 Barbara S. Peters,1,2 Andreas Beineke,3 Ulrike Maschke,4 Norbert Hosten,5 John J. Mullins,6 and Rainer Rettig1,2

Institutes of1Physiology and 5Diagnostic Radiology and Neuroradiology, 2Department of Cardiovascular Medicine, University of Greifswald, Greifswald; 3Institute of Pathology, University of Veterinary Medicine Hannover, Hannover; 4Max Delbrück Center for Molecular Medicine, Berlin-Buch, Germany; and 6Molecular Physiology Laboratory, University of Edinburgh, Edinburgh, United Kingdom

Submitted October 28, 2008 ; accepted in final form September 9, 2009

The aim of the present study was to test the hypothesis that elevation of prorenin in plasma is sufficient to induce cardiac fibrosis. Normotensive cyp1a1ren-2 transgenic rats with normal plasma prorenin and aldosterone levels were given 0.125% indole-3-carbinol (I3C) orally for a period of 12 wk. Plasma prorenin and aldosterone levels were determined in 4-wk intervals, and cardiac marker enzymes for hypertrophy, fibrosis, and oxidative stress as well as cardiac pathology were investigated. In I3C-treated cyp1a1 ren-2 transgenic rats, plasma prorenin concentrations were >100-fold elevated (≥7.1 ± 2.6 µg ANG I·ml–1·h–1 vs. ≤0.07 ± 0.1; P < 0.001), whereas active renin levels were suppressed (0.09 ± 0.02 vs. 0.2 ± 0.1; P < 0.05). Aldosterone concentrations were elevated three- to fourfold for a period of >4 wk (574 ± 51 vs. 160 ± 68 pg/ml; P < 0.01). After 12 wk of I3C, rats exhibited moderate cardiac hypertrophy (heart weight/body weight 2.5 ± 0.04 vs. 3.1 ± 0.1 mg/g; P < 0.01). There was a slight increase in mRNA contents of endothelin 1 (1.21 ± 0.08 vs. 0.75 ± 0.007; P < 0.001), NADP oxidase-2 (1.03 ± 0.006 vs. 0.76 ± 0.04; P < 0.001), transforming growth factor-β (0.99 ± 0.06 vs. 0.84 ± 0.04; P < 0.05), collagen type I (1.32 ± 0.32 vs. 0.94 ± 0.18; P < 0.05), and intercellular adhesion molecule-1 (1.12 ± 0.12 vs. 0.84 ± 0.08; P < 0.05). These genes are known to be stimulated by the renin-angiotensin system. There were no histological signs of fibrosis in the heart. We found that prorenin and aldosterone alone are not sufficient to induce considerable cardiac fibrosis in the absence of sodium load.

prorenin; aldosterone; cardiac fibrosis; renin receptor


Address for reprint requests and other correspondence: J. Peters, Institute of Physiology, Univ. of Greifswald, Greifswalder Str. 11C, D-17495 Karlsburg, Germany (e-mail: joerg.peters{at}uni-greifswald.de).






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