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Antihypertensive Role of Tissue Kallikrein in Hyperaldosteronism in the Mouse

Tissue kallikrein (TK) is synthesized in arteries and distal renal tubule, the main target of aldosterone. Urinary kallikrein excretion increases in hyperaldosteronism. We tested the hypothesis that TK is involved in the cardiovascular and renal effects of high aldosterone. Kallikrein-deficient mice... Full description

Journal Title: Endocrinology (Philadelphia) 2012-08, Vol.153 (8), p.3886-3896
Main Author: Waeckel, Ludovic
Other Authors: Potier, Louis , Chollet, Catherine , Taveau, Christopher , Bruneval, Patrick , Roussel, Ronan , Alhenc-Gelas, François , Bouby, Nadine
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Chevy Chase, MD: Endocrine Society
ID: ISSN: 0013-7227
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recordid: cdi_proquest_miscellaneous_1027679948
title: Antihypertensive Role of Tissue Kallikrein in Hyperaldosteronism in the Mouse
format: Article
creator:
  • Waeckel, Ludovic
  • Potier, Louis
  • Chollet, Catherine
  • Taveau, Christopher
  • Bruneval, Patrick
  • Roussel, Ronan
  • Alhenc-Gelas, François
  • Bouby, Nadine
subjects:
  • Abridged Index Medicus
  • Adrenals. Adrenal axis. Renin-angiotensin system (diseases)
  • Aldosterone - blood
  • Aldosterone - therapeutic use
  • Animals
  • Antihypertensive Agents - therapeutic use
  • Biological and medical sciences
  • Blood Pressure - drug effects
  • Endocrinopathies
  • Fundamental and applied biological sciences. Psychology
  • Hyperaldosteronism - diet therapy
  • Hyperaldosteronism - drug therapy
  • Hyperaldosteronism - genetics
  • Hyperaldosteronism - metabolism
  • Male
  • Medical sciences
  • Mice
  • Non tumoral diseases. Target tissue resistance. Benign neoplasms
  • Renin - genetics
  • Renin - metabolism
  • Sodium Chloride - therapeutic use
  • Sodium Chloride, Dietary - therapeutic use
  • Tissue Kallikreins - genetics
  • Tissue Kallikreins - metabolism
  • Vertebrates: endocrinology
ispartof: Endocrinology (Philadelphia), 2012-08, Vol.153 (8), p.3886-3896
description: Tissue kallikrein (TK) is synthesized in arteries and distal renal tubule, the main target of aldosterone. Urinary kallikrein excretion increases in hyperaldosteronism. We tested the hypothesis that TK is involved in the cardiovascular and renal effects of high aldosterone. Kallikrein-deficient mice (TK−/−), and wild-type (WT) littermates, studied on two different genetic backgrounds, were treated with aldosterone and high-NaCl diet for 1 month. Control mice received vehicle and standard NaCl diet. Treatment induced 5- to 7-fold increase in plasma aldosterone, suppressed renin secretion, and increased urinary TK activity. In 129SvJ-C57BL/6J mice, blood pressure monitored by radiotelemetry was not different between control TK−/− and WT mice. In TK−/− mice, aldosterone induced larger increases in blood pressure than in WT mice (+47 vs. +27 mm Hg; genotype-treatment interaction, P < 0.05). Night-day difference was also exacerbated in treated TK−/− mice (P < 0.01). Moderate cardiac septal hypertrophy was observed in hypertensive animals without major change in heart function. Aldosterone-salt increased kidney weight similarly in both genotypes but induced a 2-fold increase in renal mRNA abundance of epithelial sodium channel subunits only in TK−/− mice. The hypertensive effect of TK deficiency was also documented in treated C57BL/6J mice. In this strain, aldosterone-induced hypertension was only observed in TK−/− mice (+16 mm Hg, P < 0.01). These findings show that TK deficiency exacerbates aldosterone-salt-induced hypertension. This effect may be due at least in part to enhanced sodium reabsorption in the distal nephron aggravating sodium retention. The study suggests that kallikrein plays an antihypertensive role in hyperaldosteronism.
language: eng
source:
identifier: ISSN: 0013-7227
fulltext: no_fulltext
issn:
  • 0013-7227
  • 1945-7170
url: Link


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titleAntihypertensive Role of Tissue Kallikrein in Hyperaldosteronism in the Mouse
creatorWaeckel, Ludovic ; Potier, Louis ; Chollet, Catherine ; Taveau, Christopher ; Bruneval, Patrick ; Roussel, Ronan ; Alhenc-Gelas, François ; Bouby, Nadine
creatorcontribWaeckel, Ludovic ; Potier, Louis ; Chollet, Catherine ; Taveau, Christopher ; Bruneval, Patrick ; Roussel, Ronan ; Alhenc-Gelas, François ; Bouby, Nadine
descriptionTissue kallikrein (TK) is synthesized in arteries and distal renal tubule, the main target of aldosterone. Urinary kallikrein excretion increases in hyperaldosteronism. We tested the hypothesis that TK is involved in the cardiovascular and renal effects of high aldosterone. Kallikrein-deficient mice (TK−/−), and wild-type (WT) littermates, studied on two different genetic backgrounds, were treated with aldosterone and high-NaCl diet for 1 month. Control mice received vehicle and standard NaCl diet. Treatment induced 5- to 7-fold increase in plasma aldosterone, suppressed renin secretion, and increased urinary TK activity. In 129SvJ-C57BL/6J mice, blood pressure monitored by radiotelemetry was not different between control TK−/− and WT mice. In TK−/− mice, aldosterone induced larger increases in blood pressure than in WT mice (+47 vs. +27 mm Hg; genotype-treatment interaction, P < 0.05). Night-day difference was also exacerbated in treated TK−/− mice (P < 0.01). Moderate cardiac septal hypertrophy was observed in hypertensive animals without major change in heart function. Aldosterone-salt increased kidney weight similarly in both genotypes but induced a 2-fold increase in renal mRNA abundance of epithelial sodium channel subunits only in TK−/− mice. The hypertensive effect of TK deficiency was also documented in treated C57BL/6J mice. In this strain, aldosterone-induced hypertension was only observed in TK−/− mice (+16 mm Hg, P < 0.01). These findings show that TK deficiency exacerbates aldosterone-salt-induced hypertension. This effect may be due at least in part to enhanced sodium reabsorption in the distal nephron aggravating sodium retention. The study suggests that kallikrein plays an antihypertensive role in hyperaldosteronism.
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subjectAbridged Index Medicus ; Adrenals. Adrenal axis. Renin-angiotensin system (diseases) ; Aldosterone - blood ; Aldosterone - therapeutic use ; Animals ; Antihypertensive Agents - therapeutic use ; Biological and medical sciences ; Blood Pressure - drug effects ; Endocrinopathies ; Fundamental and applied biological sciences. Psychology ; Hyperaldosteronism - diet therapy ; Hyperaldosteronism - drug therapy ; Hyperaldosteronism - genetics ; Hyperaldosteronism - metabolism ; Male ; Medical sciences ; Mice ; Non tumoral diseases. Target tissue resistance. Benign neoplasms ; Renin - genetics ; Renin - metabolism ; Sodium Chloride - therapeutic use ; Sodium Chloride, Dietary - therapeutic use ; Tissue Kallikreins - genetics ; Tissue Kallikreins - metabolism ; Vertebrates: endocrinology
ispartofEndocrinology (Philadelphia), 2012-08, Vol.153 (8), p.3886-3896
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1Potier, Louis
2Chollet, Catherine
3Taveau, Christopher
4Bruneval, Patrick
5Roussel, Ronan
6Alhenc-Gelas, François
7Bouby, Nadine
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0Antihypertensive Role of Tissue Kallikrein in Hyperaldosteronism in the Mouse
1Endocrinology (Philadelphia)
addtitleEndocrinology
descriptionTissue kallikrein (TK) is synthesized in arteries and distal renal tubule, the main target of aldosterone. Urinary kallikrein excretion increases in hyperaldosteronism. We tested the hypothesis that TK is involved in the cardiovascular and renal effects of high aldosterone. Kallikrein-deficient mice (TK−/−), and wild-type (WT) littermates, studied on two different genetic backgrounds, were treated with aldosterone and high-NaCl diet for 1 month. Control mice received vehicle and standard NaCl diet. Treatment induced 5- to 7-fold increase in plasma aldosterone, suppressed renin secretion, and increased urinary TK activity. In 129SvJ-C57BL/6J mice, blood pressure monitored by radiotelemetry was not different between control TK−/− and WT mice. In TK−/− mice, aldosterone induced larger increases in blood pressure than in WT mice (+47 vs. +27 mm Hg; genotype-treatment interaction, P < 0.05). Night-day difference was also exacerbated in treated TK−/− mice (P < 0.01). Moderate cardiac septal hypertrophy was observed in hypertensive animals without major change in heart function. Aldosterone-salt increased kidney weight similarly in both genotypes but induced a 2-fold increase in renal mRNA abundance of epithelial sodium channel subunits only in TK−/− mice. The hypertensive effect of TK deficiency was also documented in treated C57BL/6J mice. In this strain, aldosterone-induced hypertension was only observed in TK−/− mice (+16 mm Hg, P < 0.01). These findings show that TK deficiency exacerbates aldosterone-salt-induced hypertension. This effect may be due at least in part to enhanced sodium reabsorption in the distal nephron aggravating sodium retention. The study suggests that kallikrein plays an antihypertensive role in hyperaldosteronism.
subject
0Abridged Index Medicus
1Adrenals. Adrenal axis. Renin-angiotensin system (diseases)
2Aldosterone - blood
3Aldosterone - therapeutic use
4Animals
5Antihypertensive Agents - therapeutic use
6Biological and medical sciences
7Blood Pressure - drug effects
8Endocrinopathies
9Fundamental and applied biological sciences. Psychology
10Hyperaldosteronism - diet therapy
11Hyperaldosteronism - drug therapy
12Hyperaldosteronism - genetics
13Hyperaldosteronism - metabolism
14Male
15Medical sciences
16Mice
17Non tumoral diseases. Target tissue resistance. Benign neoplasms
18Renin - genetics
19Renin - metabolism
20Sodium Chloride - therapeutic use
21Sodium Chloride, Dietary - therapeutic use
22Tissue Kallikreins - genetics
23Tissue Kallikreins - metabolism
24Vertebrates: endocrinology
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titleAntihypertensive Role of Tissue Kallikrein in Hyperaldosteronism in the Mouse
authorWaeckel, Ludovic ; Potier, Louis ; Chollet, Catherine ; Taveau, Christopher ; Bruneval, Patrick ; Roussel, Ronan ; Alhenc-Gelas, François ; Bouby, Nadine
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1Adrenals. Adrenal axis. Renin-angiotensin system (diseases)
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3Aldosterone - therapeutic use
4Animals
5Antihypertensive Agents - therapeutic use
6Biological and medical sciences
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12Hyperaldosteronism - genetics
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18Renin - genetics
19Renin - metabolism
20Sodium Chloride - therapeutic use
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22Tissue Kallikreins - genetics
23Tissue Kallikreins - metabolism
24Vertebrates: endocrinology
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2Chollet, Catherine
3Taveau, Christopher
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7Bouby, Nadine
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abstractTissue kallikrein (TK) is synthesized in arteries and distal renal tubule, the main target of aldosterone. Urinary kallikrein excretion increases in hyperaldosteronism. We tested the hypothesis that TK is involved in the cardiovascular and renal effects of high aldosterone. Kallikrein-deficient mice (TK−/−), and wild-type (WT) littermates, studied on two different genetic backgrounds, were treated with aldosterone and high-NaCl diet for 1 month. Control mice received vehicle and standard NaCl diet. Treatment induced 5- to 7-fold increase in plasma aldosterone, suppressed renin secretion, and increased urinary TK activity. In 129SvJ-C57BL/6J mice, blood pressure monitored by radiotelemetry was not different between control TK−/− and WT mice. In TK−/− mice, aldosterone induced larger increases in blood pressure than in WT mice (+47 vs. +27 mm Hg; genotype-treatment interaction, P < 0.05). Night-day difference was also exacerbated in treated TK−/− mice (P < 0.01). Moderate cardiac septal hypertrophy was observed in hypertensive animals without major change in heart function. Aldosterone-salt increased kidney weight similarly in both genotypes but induced a 2-fold increase in renal mRNA abundance of epithelial sodium channel subunits only in TK−/− mice. The hypertensive effect of TK deficiency was also documented in treated C57BL/6J mice. In this strain, aldosterone-induced hypertension was only observed in TK−/− mice (+16 mm Hg, P < 0.01). These findings show that TK deficiency exacerbates aldosterone-salt-induced hypertension. This effect may be due at least in part to enhanced sodium reabsorption in the distal nephron aggravating sodium retention. The study suggests that kallikrein plays an antihypertensive role in hyperaldosteronism.
copChevy Chase, MD
pubEndocrine Society
pmid22669897
doi10.1210/en.2012-1225
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