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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3 Pt 2
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pubmed:dateCreated |
1998-4-14
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pubmed:abstractText |
Ureteral obstruction causes infiltration of the kidney by monocytes/macrophages. This infiltrate is significantly reduced by administration of an angiotensin-converting enzyme (ACE) inhibitor but not by a specific angiotensin II type 1 receptor (AT1 receptor) antagonist. Chemoattractants and cell surface adhesive molecules mediate monocyte/macrophage infiltration. Rats with unilateral ureteral obstruction (UUO) of 1, 3, or 5 days duration were untreated or given enalapril or SC-51316 in the drinking water. We measured the mRNA levels of monocyte chemoatactic peptide 1 (MCP-1), a chemoattractant, and levels of intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1), two cell surface adhesion proteins. MCP-1 mRNA increased significantly after 1 day of UUO and increased further through 5 days of UUO in the obstructed kidney. ICAM-1 mRNA also increased significantly after 1 day but steadily declined through 5 days of UUO in the obstructed kidney. VCAM-1 mRNA did not increase significantly until after 3 days of UUO and increased further through 5 days of obstruction. Enalapril or SC-51316 treatment had no significant effect on ICAM-1 mRNA levels. MCP-1 mRNA levels were reduced but remained significantly elevated. Enalapril significantly blunted the increase in VCAM-1 mRNA levels and VCAM-1 protein determined by immunocytochemistry; SC-51316 had no significant effect. Thus changes in VCAM-1 levels may account for the differential effect of enalapril and SC-51316 on monocyte/macrophage infiltration of the kidney during ureteral obstruction.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Cell Adhesion Molecules,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Enalapril,
http://linkedlifedata.com/resource/pubmed/chemical/Intercellular Adhesion Molecule-1,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 2,
http://linkedlifedata.com/resource/pubmed/chemical/SC 51316,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Triazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Vascular Cell Adhesion Molecule-1
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0002-9513
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
F580-6
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:9530275-Angiotensin Receptor Antagonists,
pubmed-meshheading:9530275-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:9530275-Animals,
pubmed-meshheading:9530275-Cell Adhesion,
pubmed-meshheading:9530275-Cell Adhesion Molecules,
pubmed-meshheading:9530275-Chemokine CCL2,
pubmed-meshheading:9530275-Enalapril,
pubmed-meshheading:9530275-Female,
pubmed-meshheading:9530275-Gene Expression Regulation,
pubmed-meshheading:9530275-Immunohistochemistry,
pubmed-meshheading:9530275-Intercellular Adhesion Molecule-1,
pubmed-meshheading:9530275-Macrophages,
pubmed-meshheading:9530275-Monocytes,
pubmed-meshheading:9530275-RNA, Messenger,
pubmed-meshheading:9530275-Rats,
pubmed-meshheading:9530275-Rats, Sprague-Dawley,
pubmed-meshheading:9530275-Receptor, Angiotensin, Type 1,
pubmed-meshheading:9530275-Receptor, Angiotensin, Type 2,
pubmed-meshheading:9530275-Tetrazoles,
pubmed-meshheading:9530275-Triazoles,
pubmed-meshheading:9530275-Ureteral Obstruction,
pubmed-meshheading:9530275-Vascular Cell Adhesion Molecule-1
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pubmed:year |
1998
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pubmed:articleTitle |
Differential effects of ACE and AT1 receptor inhibition on chemoattractant and adhesion molecule synthesis.
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pubmed:affiliation |
Department of Medicine, Washington University School of Medicine at Barnes-Jewish Hospital, St. Louis, Missouri 63110, USA. morrisse@imgate.wustl.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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