Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-9-24
pubmed:abstractText
Upper body obesity is associated with insulin resistance, hypertension, and endothelial dysfunction. We examined forearm vascular function in response to vasodilator (endothelium-dependent and endothelium-independent) and vasoconstrictor stimuli in 8 normotensive, upper body/viscerally obese men with a positive family history of hypertension and 8 age-matched nonobese men. We also measured body composition and insulin regulation of free fatty acid (FFA) and glucose metabolism. Forearm blood flow was measured before and during brachial artery infusions of acetylcholine (Ach), sodium nitroprusside (NTP), and angiotensin II (+/-nitric oxide synthase [NO]) synthase blockade with N(G)-monomethyl L-arginine [L-NMMA]). On a separate day, baseline and insulin-regulated glucose ([3-3H]glucose) and FFA ([9,10-3H]palmitate) turnover were measured. The vasoconstrictor response to angiotensin II was greater (P<0.05) in obese men than in nonobese men, whereas endothelium-dependent vasodilation was similar. The slope of the angiotensin II dose-response curve correlated significantly with the basal plasma palmitate concentration. Basal and insulin-mediated glucose disposal was significantly reduced and FFA turnover significantly increased in viscerally obese men. No differences in endothelium-independent vasodilation or relationships between vascular responsivity and palmitate and glucose kinetics or body composition were found. Angiotensin II-stimulated forearm vasoconstriction is increased in viscerally obese normotensive men.
pubmed:grant
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
44
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
435-41
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15337733-Acetylcholine, pubmed-meshheading:15337733-Adult, pubmed-meshheading:15337733-Angiotensin II, pubmed-meshheading:15337733-Blood Glucose, pubmed-meshheading:15337733-Body Composition, pubmed-meshheading:15337733-Dose-Response Relationship, Drug, pubmed-meshheading:15337733-Forearm, pubmed-meshheading:15337733-Humans, pubmed-meshheading:15337733-Hypertension, pubmed-meshheading:15337733-Insulin Resistance, pubmed-meshheading:15337733-Lipolysis, pubmed-meshheading:15337733-Male, pubmed-meshheading:15337733-Nitric Oxide Synthase, pubmed-meshheading:15337733-Nitroprusside, pubmed-meshheading:15337733-Obesity, pubmed-meshheading:15337733-Palmitic Acid, pubmed-meshheading:15337733-Regional Blood Flow, pubmed-meshheading:15337733-Vasoconstriction, pubmed-meshheading:15337733-Vasoconstrictor Agents, pubmed-meshheading:15337733-Vasodilation, pubmed-meshheading:15337733-Vasodilator Agents, pubmed-meshheading:15337733-omega-N-Methylarginine
pubmed:year
2004
pubmed:articleTitle
Vascular response to angiotensin II in upper body obesity.
pubmed:affiliation
Endocrine Research Unit, Mayo Clinic, Rochester, Minn 55905, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't