PMID- 9530275
OWN - NLM
STAT- MEDLINE
DCOM- 19980414
LR  - 20190416
IS  - 0002-9513 (Print)
IS  - 0002-9513 (Linking)
VI  - 274
IP  - 3
DP  - 1998 Mar
TI  - Differential effects of ACE and AT1 receptor inhibition on chemoattractant and 
      adhesion molecule synthesis.
PG  - F580-6
LID - 10.1152/ajprenal.1998.274.3.F580 [doi]
AB  - 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.
FAU - Morrissey, J J
AU  - Morrissey JJ
AD  - Department of Medicine, Washington University School of Medicine at Barnes-Jewish 
      Hospital, St. Louis, Missouri 63110, USA. morrisse@imgate.wustl.edu
FAU - Klahr, S
AU  - Klahr S
LA  - eng
GR  - DK-09976/DK/NIDDK NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Physiol
JT  - The American journal of physiology
JID - 0370511
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Angiotensin-Converting Enzyme Inhibitors)
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptor, Angiotensin, Type 2)
RN  - 0 (Tetrazoles)
RN  - 0 (Triazoles)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 133690-62-7 (SC 51316)
RN  - 69PN84IO1A (Enalapril)
SB  - IM
MH  - *Angiotensin Receptor Antagonists
MH  - Angiotensin-Converting Enzyme Inhibitors/*pharmacology
MH  - Animals
MH  - Cell Adhesion
MH  - Cell Adhesion Molecules/biosynthesis
MH  - Chemokine CCL2/*biosynthesis
MH  - Enalapril/pharmacology
MH  - Female
MH  - Gene Expression Regulation/drug effects
MH  - Immunohistochemistry
MH  - Intercellular Adhesion Molecule-1/*biosynthesis
MH  - Macrophages/cytology
MH  - Monocytes/cytology
MH  - RNA, Messenger/genetics
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Angiotensin, Type 1
MH  - Receptor, Angiotensin, Type 2
MH  - Tetrazoles/pharmacology
MH  - Triazoles/pharmacology
MH  - Ureteral Obstruction/physiopathology
MH  - Vascular Cell Adhesion Molecule-1/*biosynthesis
EDAT- 1998/04/08 00:00
MHDA- 1998/04/08 00:01
CRDT- 1998/04/08 00:00
PHST- 1998/04/08 00:00 [pubmed]
PHST- 1998/04/08 00:01 [medline]
PHST- 1998/04/08 00:00 [entrez]
AID - 10.1152/ajprenal.1998.274.3.F580 [doi]
PST - ppublish
SO  - Am J Physiol. 1998 Mar;274(3):F580-6. doi: 10.1152/ajprenal.1998.274.3.F580.