Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism

J. Peters, T. Schluter, T. Riegel, B. S. Peters, A. Beineke, U. Maschke, N. Hosten, J. J. Mullins, R. Rettig

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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 mu g ANG I . ml(-1) . h(-1) vs. 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-beta (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.
Original languageEnglish
Pages (from-to)H1845-H1852
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number5
Publication statusPublished - Nov 2009


  • prorenin
  • aldosterone
  • cardiac fibrosis
  • renin receptor


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