Linked Life Data

16087779

Source:http://linkedlifedata.com/resource/pubmed/id/16087779

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2005-9-30
pubmed:abstractText
It is known that the endothelial function is compromised in atherosclerosis and arterial hypertension and that angiotensin is an important factor contributing to both pathophysiologies. The aim of this study was to evaluate the vascular function in a hypercholesterolemia/atherosclerosis model, in the angiotensin II-dependent 2-kidney 1-clip (2K1C) hypertension model and when both conditions coexist. Eight-week-old apolipoprotein E knockout (apoE; n=20) and C57BL/6 (C57; n=20) mice underwent a 2K1C or sham operation and were studied 28 days later. Mean arterial pressure was higher in apoE-2K1C and C57-2K1C (126+/-3 and 128+/-3 mm Hg) when compared with the apoE-Sham and C57-Sham (103+/-2 and 104+/-2 mm Hg, respectively; P<0.05). The vascular reactivity to norepinephrine (NE; 10(-9) to 2 x 10(-3) mol/L), acetylcholine (ACh), and sodium nitroprusside (SNP; 10(-10) to 10(-3) mol/L) was evaluated in the mesenteric arteriolar bed through concentration-effect curves. NE caused vascular hyper-reactivity in apoE-Sham, apoE-2K1C, and C57-2K1C (maximal response 146+/-5, 144+/-5, and 159+/-4 mm Hg, respectively) compared with C57-Sham (122+/-7 mm Hg; P<0.05). The ACh-induced relaxation was smaller (P<0.05) in apoE-2K1C and C57-2K1C (maximal response 53+/-3% and 46+/-3%) than in apoE-Sham and C57-Sham mice (78+/-5% and 73+/-4%). SNP-induced vascular relaxation showed similar concentration-effect curves in all groups. We conclude that in C57-2K1C mice, the increased reactivity to NE and the decreased endothelium-dependent relaxation contribute to the maintenance of hypertension. The apoE mouse, at early stages of atherosclerosis, shows hyper-reactivity to NE but does not have endothelium dysfunction yet. However, the concurrence of both pathophysiologies does not result in additive effects on the vascular function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1524-4563
pubmed:author
pubmed:issnType
Electronic
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
932-6
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:16087779-Acetylcholine, pubmed-meshheading:16087779-Angiotensins, pubmed-meshheading:16087779-Animals, pubmed-meshheading:16087779-Apolipoproteins E, pubmed-meshheading:16087779-Atherosclerosis, pubmed-meshheading:16087779-Blood Pressure, pubmed-meshheading:16087779-Blood Vessels, pubmed-meshheading:16087779-Dose-Response Relationship, Drug, pubmed-meshheading:16087779-Hypercholesterolemia, pubmed-meshheading:16087779-Hypertension, Renovascular, pubmed-meshheading:16087779-Male, pubmed-meshheading:16087779-Mice, pubmed-meshheading:16087779-Mice, Knockout, pubmed-meshheading:16087779-Nitroprusside, pubmed-meshheading:16087779-Norepinephrine, pubmed-meshheading:16087779-Vasoconstriction, pubmed-meshheading:16087779-Vasoconstrictor Agents, pubmed-meshheading:16087779-Vasodilation, pubmed-meshheading:16087779-Vasodilator Agents
pubmed:year
2005
pubmed:articleTitle
Evaluation of vascular function in apolipoprotein E knockout mice with angiotensin-dependent renovascular hypertension.
pubmed:affiliation
Laboratory of Transgenes and Cardiovascular Control, Biomedical Center, Federal University of Espirito Santo, Brazil.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't