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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Angiotensin Inhibition Reduces Glomerular Damage and Renal Chemokine Expression in MRL/lpr Mice

Guillermo Pérez de Lema, Cor de Wit, Clemens D. Cohen, Elena Nieto, Ana Molina, Bernhard Banas, Bruno Luckow, Ana B. Vicente, Francisco Mampaso and Detlef Schlöndorff
Journal of Pharmacology and Experimental Therapeutics October 2003, 307 (1) 275-281; DOI: https://doi.org/10.1124/jpet.103.053678
Guillermo Pérez de Lema
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Cor de Wit
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Clemens D. Cohen
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Elena Nieto
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Ana Molina
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Bernhard Banas
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Bruno Luckow
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Ana B. Vicente
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Francisco Mampaso
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Detlef Schlöndorff
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Abstract

Beneficial effects of angiotensin II inhibition during inflammatory renal disease may involve both hemodynamic and nonhemodynamic mechanisms. To analyze whether angiotensin II inhibition has protective effects on lupus-like, autoimmune-mediated renal damage in MRL/lpr mice, four groups of mice were treated orally for 6 weeks with: 1) vehicle, 2) enalapril (3.0 mg/kg per day), 3) candesartan cilexetil (5.0 mg/kg), or 4) amlodipine (10 mg/kg) as a blood pressure control (n = 9–12/group). All antihypertensive treatments lowered blood pressure to a similar level compared with vehicle group (enalapril: 99.8 ± 8.3 mm Hg; candesartan: 101 ± 9 mm Hg; amlodipine: 103.8 ± 6.7 mm Hg; vehicle: 113.5 ± 4.6 mm Hg). Vehicle-treated mice developed a moderate glomerular injury with albuminuria (35.1 ± 39.0 μg/mg of creatinine). Glomerular lesions consisted of immune complex deposition and mesangial expansion with increased mesangial cell proliferation. Amlodipine treatment had no significant protective effects. In contrast to vehicle- and amlodipine-treated mice, those subjected to angiotensin II blockade with enalapril or candesartan had reduced albuminuria, glomerular expansion, and mesangial proliferation. This was associated with significantly reduced renal chemokine mRNA expression compared with vehicle treatment. Our results show that inhibition of angiotensin II has protective effects on the glomerular damage of MRL/lpr mice that extend beyond hemodynamics and involve down-modulation of glomerular inflammation, reduction of mesangial cell proliferation, and decrease in chemokine expression.

Footnotes

  • G.P.d.L. was supported by a postdoctoral fellowship from the Spanish Ministerio de Educación y Cultura (Grant EX 97 7230290). This work was supported in part by grants from the Deutsche Forschungsgemeinschaft to B.B. and to B.L., from Takeda Chemical Industries, Ltd. to D.S., from Verum Stiftung to G.P.d.L., from Bayerischer Habilitationsförderpreis to C.D.C., and from the Fondo de Investigación Sanitaria (Grant 00/0246) and the Comunidad de Madrid (Grant 08.4/0015/98) to F.M.

  • ABBREVIATIONS: RAS, renin-angiotensin-system; ACE, angiotensin-converting enzyme; ACEI, angiotensin-converting enzyme inhibitor; MCP-1, monocyte chemotactic protein-1; BP, mean arterial blood pressure; ELISA, enzyme-linked immunosorbent assay; RPA, ribonuclease protection assay; IC, immune complex; CCL, CC chemokine ligand; CXCL, CXC chemokine ligand; RANTES, regulated on activation normal T cell expressed and secreted.

  • DOI: 10.1124/jpet.103.053678.

    • Received May 5, 2003.
    • Accepted June 27, 2003.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics: 307 (1)
Journal of Pharmacology and Experimental Therapeutics
Vol. 307, Issue 1
1 Oct 2003
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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Angiotensin Inhibition Reduces Glomerular Damage and Renal Chemokine Expression in MRL/lpr Mice

Guillermo Pérez de Lema, Cor de Wit, Clemens D. Cohen, Elena Nieto, Ana Molina, Bernhard Banas, Bruno Luckow, Ana B. Vicente, Francisco Mampaso and Detlef Schlöndorff
Journal of Pharmacology and Experimental Therapeutics October 1, 2003, 307 (1) 275-281; DOI: https://doi.org/10.1124/jpet.103.053678

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Research ArticleINFLAMMATION AND IMMUNOPHARMACOLOGY

Angiotensin Inhibition Reduces Glomerular Damage and Renal Chemokine Expression in MRL/lpr Mice

Guillermo Pérez de Lema, Cor de Wit, Clemens D. Cohen, Elena Nieto, Ana Molina, Bernhard Banas, Bruno Luckow, Ana B. Vicente, Francisco Mampaso and Detlef Schlöndorff
Journal of Pharmacology and Experimental Therapeutics October 1, 2003, 307 (1) 275-281; DOI: https://doi.org/10.1124/jpet.103.053678
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