PMID- 12626661
OWN - NLM
STAT- MEDLINE
DCOM- 20030707
LR  - 20220317
IS  - 0022-3565 (Print)
IS  - 0022-3565 (Linking)
VI  - 305
IP  - 3
DP  - 2003 Jun
TI  - Angiotensin II type 1 receptor antagonists inhibit basal as well as low-density 
      lipoprotein and platelet-activating factor-stimulated human monocyte 
      chemoattractant protein-1.
PG  - 846-53
AB  - Monocyte chemoattractant protein-1 (MCP-1) is a potent chemotactic agent for 
      monocytes and other cells and is thought to be involved in atherosclerosis, 
      recruiting monocytes to the subendothelial space or to the site of inflammation. 
      Angiotensin II has been demonstrated, at least in animal models, to stimulate 
      MCP-1 expression. We investigated the effect of the angiotensin II type 1 (AT1) 
      receptor antagonists irbesartan and losartan on MCP-1 production by freshly 
      isolated human monocytes. Irbesartan and losartan inhibited basal MCP-1 
      production in a dose-dependent manner. Low-density lipoprotein (LDL) stimulated 
      MCP-1 in a concentration-dependent manner, with 200 microg/ml LDL protein giving 
      a 2-fold increase in MCP-1. Irbesartan and losartan dose dependently blocked 
      LDL-stimulated MCP-1. An angiotensin II type 2 receptor antagonist, 
      S-(+)-1-([4-(dimethylamino)-3-methylphenyl]methyl)-5-(diphenylacetyl)-4,5,6,7-tetrahydro-1H-imidazo(4,5-c)pyridine-6-carboxylic 
      acid (PD123319), had no significant effect on basal MCP-1 levels or 
      LDL-stimulated MCP-1. After noting homology between the AT1 receptor and the 
      platelet-activating factor (PAF) receptor, we showed that irbesartan inhibited 
      both [3H]PAF binding to human monocytes and carbamyl-PAF stimulation of MCP-1. 
      However, irbesartan affinity for the PAF receptor was 700 times less than PAF, 
      suggesting that there may be another mechanism for irbesartan inhibition of 
      PAF-stimulated MCP-1. This is the first report showing that AT1 receptor 
      antagonists inhibit basal as well as LDL- and PAF-stimulated MCP-1 production in 
      freshly isolated human monocytes.
FAU - Proudfoot, Julie M
AU  - Proudfoot JM
AD  - Department of Medicine, University of Western Australia and the West Australian 
      Institute for Medical Research, Perth, Australia. jproudft@cyllene.uwa.edu.au
FAU - Croft, Kevin D
AU  - Croft KD
FAU - Puddey, Ian B
AU  - Puddey IB
FAU - Beilin, Lawrence J
AU  - Beilin LJ
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20030306
PL  - United States
TA  - J Pharmacol Exp Ther
JT  - The Journal of pharmacology and experimental therapeutics
JID - 0376362
RN  - 0 (Angiotensin Receptor Antagonists)
RN  - 0 (Antihypertensive Agents)
RN  - 0 (Biphenyl Compounds)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Platelet Activating Factor)
RN  - 0 (Platelet Membrane Glycoproteins)
RN  - 0 (Receptor, Angiotensin, Type 1)
RN  - 0 (Receptors, Cell Surface)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Tetrazoles)
RN  - 0 (platelet activating factor receptor)
RN  - J0E2756Z7N (Irbesartan)
RN  - JMS50MPO89 (Losartan)
SB  - IM
MH  - *Angiotensin Receptor Antagonists
MH  - Antihypertensive Agents/*pharmacology
MH  - Binding Sites
MH  - Binding, Competitive
MH  - Biphenyl Compounds/*pharmacology
MH  - Chemokine CCL2/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Humans
MH  - In Vitro Techniques
MH  - Irbesartan
MH  - Lipoproteins, LDL/metabolism
MH  - Losartan/pharmacology
MH  - Monocytes/*drug effects/metabolism
MH  - Platelet Activating Factor/*metabolism
MH  - Platelet Membrane Glycoproteins/antagonists & inhibitors
MH  - Receptor, Angiotensin, Type 1
MH  - Receptors, Cell Surface/antagonists & inhibitors
MH  - *Receptors, G-Protein-Coupled
MH  - Tetrazoles/*pharmacology
EDAT- 2003/03/11 04:00
MHDA- 2003/07/08 05:00
CRDT- 2003/03/11 04:00
PHST- 2003/03/11 04:00 [pubmed]
PHST- 2003/07/08 05:00 [medline]
PHST- 2003/03/11 04:00 [entrez]
AID - jpet.102.047795 [pii]
AID - 10.1124/jpet.102.047795 [doi]
PST - ppublish
SO  - J Pharmacol Exp Ther. 2003 Jun;305(3):846-53. doi: 10.1124/jpet.102.047795. Epub 
      2003 Mar 6.