Linked Life Data

19666838

Source:http://linkedlifedata.com/resource/pubmed/id/19666838

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-9-25
pubmed:abstractText
Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonists have been shown to protect the cerebral vasculature, including the blood-brain barrier. In the present study, we investigated the effect of the PPAR-gamma agonist rosiglitazone on changes in venous permeability during chronic hypertension induced by nitric oxide synthase inhibition. Female Sprague-Dawley rats were either treated with N(G)-nitro-L-arginine methyl ester (L-NAME; 0.5 g/l in drinking water) for 5 wk (HTN; n = 8), L-NAME for 5 wk plus the PPAR-gamma agonist rosiglitazone (20 mg/kg in food) for the last 3 wk (HTN + Rosi; n = 5), L-NAME for 5 wk plus the superoxide dismutase mimetic Tempol (1 mmol/l in drinking water) for the last 3 wk (HTN + Tempol; n = 8), or were untreated controls (n = 9). Fluid filtration (J(v)/S) and hydraulic conductivity (L(p)) of cerebral veins were compared in vitro between groups after a step increase in pressure from 10 to 25 mmHg to mimic the change in hydrostatic pressure during acute hypertension. Hypertension increased J(v)/S by 2.2-fold and L(p) by 3.2-fold. Rosiglitazone treatment after 2 wk of hypertension completely reversed the increased J(v)/S and L(p) that occurred during hypertension, whereas Tempol had no effect. These results demonstrate that rosiglitazone was effective at reversing changes in venous permeability that occurred during chronic hypertension, an effect that does not appear to be related to its antioxidant properties. Our findings suggest that PPAR-gamma may be a key regulator of blood-brain barrier permeability and a potential therapeutic target during hypertension.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1522-1539
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
297
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1347-53
pubmed:dateRevised
2011-8-12
pubmed:meshHeading
pubmed-meshheading:19666838-Animals, pubmed-meshheading:19666838-Antihypertensive Agents, pubmed-meshheading:19666838-Antioxidants, pubmed-meshheading:19666838-Blood Pressure, pubmed-meshheading:19666838-Brain Edema, pubmed-meshheading:19666838-Capillary Permeability, pubmed-meshheading:19666838-Cerebral Veins, pubmed-meshheading:19666838-Cerebrovascular Circulation, pubmed-meshheading:19666838-Chronic Disease, pubmed-meshheading:19666838-Cyclic N-Oxides, pubmed-meshheading:19666838-Disease Models, Animal, pubmed-meshheading:19666838-Female, pubmed-meshheading:19666838-Hydrostatic Pressure, pubmed-meshheading:19666838-Hypertension, pubmed-meshheading:19666838-NG-Nitroarginine Methyl Ester, pubmed-meshheading:19666838-PPAR gamma, pubmed-meshheading:19666838-Rats, pubmed-meshheading:19666838-Rats, Sprague-Dawley, pubmed-meshheading:19666838-Spin Labels, pubmed-meshheading:19666838-Thiazolidinediones, pubmed-meshheading:19666838-Time Factors
pubmed:year
2009
pubmed:articleTitle
PPAR-gamma agonist rosiglitazone reverses increased cerebral venous hydraulic conductivity during hypertension.
pubmed:affiliation
1Departments of Neurology, Obstetrics, Gynecology and Reproductive Sciences, and Pharmacology, University of Vermont, Burlington, Vermont 05405, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural