Angiotensin II infusion ameliorates the early phase of a mesangioproliferative glomerulonephritis1 View Full Text


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Article Info

DATE

2002-03

AUTHORS

Ulrich O Wenzel, Friedrich Thaiss, Udo Helmchen, Rolf A K Stahl, Gunter Wolf

ABSTRACT

BACKGROUND: Inhibition of the renin-angiotensin system slows the progression of chronic renal disease. METHODS: To test whether angiotensin II (Ang II) infusion aggravates or ameliorates an acute glomerulonephritis, the peptide was infused (200 ng/min by osmotic minipump) in rats with an anti-thymocyte antibody-induced glomerulonephritis (ATS). RESULTS: Ang II significantly increased blood pressure. Following injection of the antibody, similar glomerular binding of rabbit IgG and rat complement C3 was detected in ATS and Ang II+ATS rats, indicating no differences in delivery and binding of the antibody. Ang II infusion, however, induced a significant reduction in glomerular monocyte infiltration, cell proliferation and matrix expansion in nephritic rats compared to rats with nephritis without Ang II. The antiproliferative effect of Ang II was inhibited by the Ang II type 1 (AT1) receptor blocker irbesartan, but not by the AT2 receptor blocker PD 123319, indicating that this effect was likely transduced by AT1 receptors. Norepinephrine infusion (600 ng/min) produced a similar degree of hypertension, but did not affect glomerular proliferation in nephritic rats. Ang II induced the glomerular expression of the cell cycle inhibitor p27KIP1 and of transforming growth factor-beta (TGF-beta) and inhibited expression of monocyte chemotactic protein 1 (MCP-1). CONCLUSION: Ang II surprisingly ameliorates glomerular monocyte infiltration, proliferation and matrix expansion in ATS nephritis. Ang II-mediated induction of cyclin kinase inhibitors and TGF-beta may contribute to the protection of the glomerulus from inflammatory injury by inducing cell cycle arrest and attenuating activation of local and recruited cells. Alternatively, Ang II might protect the kidney at least in part by less inflow of disease activators due to reduction of renal blood flow. Therefore, activation of the renin-angiotensin system may have protective effects in certain pathophysiological situations. More... »

PAGES

1020-1029

References to SciGraph publications

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  • 1997-03. Monocyte chemoattractant protein-1 mediates monocyte/macrophage influx in anti-thymocyte antibody-induced glomerulonephritis in KIDNEY INTERNATIONAL
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  • 1990-07. Suppression of experimental glomerulonephritis by antiserum against transforming growth factor β1 in NATURE
  • 1994-04. Macrophages in acute glomerular inflammation in KIDNEY INTERNATIONAL
  • 1999-05. The concept of glomerular self-defense in KIDNEY INTERNATIONAL
  • 1998-05. The cyclin-dependent kinase inhibitor p27Kip1 safeguards against inflammatory injury in NATURE MEDICINE
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  • 1996-12. Angiotensin II-stimulated hypertrophy of LLC-PK1 cells depends on the induction of the cyclin-dependent kinase inhibitor p27Kip1 in KIDNEY INTERNATIONAL
  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1046/j.1523-1755.2002.00192.x

    DOI

    http://dx.doi.org/10.1046/j.1523-1755.2002.00192.x

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1044077245

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/11849457


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