Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1999-5-3
pubmed:abstractText
This study investigated whether angiotensin II AT1-receptor blockade with losartan inhibits endothelium-monocyte interactions originating from long-term activation of the renin-angiotensin system in hypertensive transgenic rats [TGR(mRen2)27]. The number of circulating activated monocytes, monocytes adhered to thoracic aorta endothelium, and the extent of endothelial cell injury were compared in adult male transgenic (mRen2)27 and age-matched Hannover Sprague-Dawley (SD) rats after 12 days of continuous subcutaneous administration of saline (120 microl/24 h), losartan (10 mg/kg/24 h), or the vasodilator hydralazine (3 mg/kg/24 h). At the doses administered in this experiment, both losartan and hydralazine normalized mRen2 rat blood pressures equal to values in similarly treated SD rats. Compared with saline infusion, administration of either antihypertensive in mRen2 rats reduced (p<0.05) endothelial cell injury, but only losartan significantly (p<0.05) decreased the number of activated circulating and endothelium-adherent monocytes. Infusion of antihypertensives in SD rats had no effect on blood pressures, monocyte activity, or endothelial injury compared with saline administration. These findings suggest that the recruitment and infiltration of leukocytes into the subendothelium associated with renin-angiotensin system-induced hypertension is partly mediated by pressure-independent AT1-receptor pathways.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
341-51
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:10069667-Angiotensin II, pubmed-meshheading:10069667-Angiotensin Receptor Antagonists, pubmed-meshheading:10069667-Animals, pubmed-meshheading:10069667-Animals, Genetically Modified, pubmed-meshheading:10069667-Antihypertensive Agents, pubmed-meshheading:10069667-Blood Cell Count, pubmed-meshheading:10069667-Blood Pressure, pubmed-meshheading:10069667-Cell Adhesion, pubmed-meshheading:10069667-Endothelium, Vascular, pubmed-meshheading:10069667-Female, pubmed-meshheading:10069667-Heart Rate, pubmed-meshheading:10069667-Hematocrit, pubmed-meshheading:10069667-Hydralazine, pubmed-meshheading:10069667-Hypertension, pubmed-meshheading:10069667-Losartan, pubmed-meshheading:10069667-Male, pubmed-meshheading:10069667-Monocytes, pubmed-meshheading:10069667-Nitroblue Tetrazolium, pubmed-meshheading:10069667-Peptide Fragments, pubmed-meshheading:10069667-Rats, pubmed-meshheading:10069667-Rats, Sprague-Dawley, pubmed-meshheading:10069667-Receptor, Angiotensin, Type 1, pubmed-meshheading:10069667-Receptor, Angiotensin, Type 2, pubmed-meshheading:10069667-Renin-Angiotensin System
pubmed:year
1999
pubmed:articleTitle
Angiotensin II AT1-receptor blockade inhibits monocyte activation and adherence in transgenic (mRen2)27 rats.
pubmed:affiliation
The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Wake Forest University Baptist Medical Center, Winston-Salem, North Carolina 27157-1032, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't