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Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism
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| Zeitschriftentitel: | American Journal of Physiology-Heart and Circulatory Physiology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , |
| In: | American Journal of Physiology-Heart and Circulatory Physiology, 297, 2009, 5, S. H1845-H1852 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Peters, Jörg Schlüter, Torsten Riegel, Thomas Peters, Barbara S. Beineke, Andreas Maschke, Ulrike Hosten, Norbert Mullins, John J. Rettig, Rainer Peters, Jörg Schlüter, Torsten Riegel, Thomas Peters, Barbara S. Beineke, Andreas Maschke, Ulrike Hosten, Norbert Mullins, John J. Rettig, Rainer |
|---|---|
| author |
Peters, Jörg Schlüter, Torsten Riegel, Thomas Peters, Barbara S. Beineke, Andreas Maschke, Ulrike Hosten, Norbert Mullins, John J. Rettig, Rainer |
| spellingShingle |
Peters, Jörg Schlüter, Torsten Riegel, Thomas Peters, Barbara S. Beineke, Andreas Maschke, Ulrike Hosten, Norbert Mullins, John J. Rettig, Rainer American Journal of Physiology-Heart and Circulatory Physiology Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
| author_sort |
peters, jörg |
| spelling |
Peters, Jörg Schlüter, Torsten Riegel, Thomas Peters, Barbara S. Beineke, Andreas Maschke, Ulrike Hosten, Norbert Mullins, John J. Rettig, Rainer 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.01135.2008 <jats:p> The aim of the present study was to test the hypothesis that elevation of prorenin in plasma is sufficient to induce cardiac fibrosis. Normotensive cyp1a1 ren-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<jats:sup>−1</jats:sup>·h<jats:sup>−1</jats:sup> 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. </jats:p> Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism American Journal of Physiology-Heart and Circulatory Physiology |
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| title |
Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_unstemmed |
Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_full |
Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_fullStr |
Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_full_unstemmed |
Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_short |
Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_sort |
lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| topic |
Physiology (medical) Cardiology and Cardiovascular Medicine Physiology |
| url |
http://dx.doi.org/10.1152/ajpheart.01135.2008 |
| publishDate |
2009 |
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H1845-H1852 |
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<jats:p> The aim of the present study was to test the hypothesis that elevation of prorenin in plasma is sufficient to induce cardiac fibrosis. Normotensive cyp1a1 ren-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<jats:sup>−1</jats:sup>·h<jats:sup>−1</jats:sup> 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. </jats:p> |
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| author | Peters, Jörg, Schlüter, Torsten, Riegel, Thomas, Peters, Barbara S., Beineke, Andreas, Maschke, Ulrike, Hosten, Norbert, Mullins, John J., Rettig, Rainer |
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| description | <jats:p> The aim of the present study was to test the hypothesis that elevation of prorenin in plasma is sufficient to induce cardiac fibrosis. Normotensive cyp1a1 ren-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<jats:sup>−1</jats:sup>·h<jats:sup>−1</jats:sup> 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. </jats:p> |
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| spelling | Peters, Jörg Schlüter, Torsten Riegel, Thomas Peters, Barbara S. Beineke, Andreas Maschke, Ulrike Hosten, Norbert Mullins, John J. Rettig, Rainer 0363-6135 1522-1539 American Physiological Society Physiology (medical) Cardiology and Cardiovascular Medicine Physiology http://dx.doi.org/10.1152/ajpheart.01135.2008 <jats:p> The aim of the present study was to test the hypothesis that elevation of prorenin in plasma is sufficient to induce cardiac fibrosis. Normotensive cyp1a1 ren-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<jats:sup>−1</jats:sup>·h<jats:sup>−1</jats:sup> 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. </jats:p> Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism American Journal of Physiology-Heart and Circulatory Physiology |
| spellingShingle | Peters, Jörg, Schlüter, Torsten, Riegel, Thomas, Peters, Barbara S., Beineke, Andreas, Maschke, Ulrike, Hosten, Norbert, Mullins, John J., Rettig, Rainer, American Journal of Physiology-Heart and Circulatory Physiology, Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism, Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
| title | Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_full | Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_fullStr | Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_full_unstemmed | Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_short | Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_sort | lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| title_unstemmed | Lack of cardiac fibrosis in a new model of high prorenin hyperaldosteronism |
| topic | Physiology (medical), Cardiology and Cardiovascular Medicine, Physiology |
| url | http://dx.doi.org/10.1152/ajpheart.01135.2008 |