Document Detail


Differential effects of ACE and AT1 receptor inhibition on chemoattractant and adhesion molecule synthesis.
MedLine Citation:
PMID:  9530275     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
J J Morrissey; S Klahr
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Publication Detail:
Type:  Journal Article; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  274     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1998 Mar 
Date Detail:
Created Date:  1998-04-14     Completed Date:  1998-04-14     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  F580-6     Citation Subset:  IM    
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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MeSH Terms
Descriptor/Qualifier:
Angiotensin-Converting Enzyme Inhibitors / pharmacology*
Animals
Cell Adhesion
Cell Adhesion Molecules / biosynthesis
Chemokine CCL2 / biosynthesis*
Enalapril / pharmacology
Female
Gene Expression Regulation / drug effects
Immunohistochemistry
Intercellular Adhesion Molecule-1 / biosynthesis*
Macrophages / cytology
Monocytes / cytology
RNA, Messenger / genetics
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1
Receptor, Angiotensin, Type 2
Receptors, Angiotensin / antagonists & inhibitors*
Tetrazoles / pharmacology
Triazoles / pharmacology
Ureteral Obstruction / physiopathology
Vascular Cell Adhesion Molecule-1 / biosynthesis*
Grant Support
ID/Acronym/Agency:
DK-09976/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Angiotensin-Converting Enzyme Inhibitors; 0/Cell Adhesion Molecules; 0/Chemokine CCL2; 0/RNA, Messenger; 0/Receptor, Angiotensin, Type 1; 0/Receptor, Angiotensin, Type 2; 0/Receptors, Angiotensin; 0/Tetrazoles; 0/Triazoles; 0/Vascular Cell Adhesion Molecule-1; 126547-89-5/Intercellular Adhesion Molecule-1; 133690-62-7/SC 51316; 75847-73-3/Enalapril

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