Document Detail


The vascular renin-angiotensin system contributes to blunted vasodilation induced by transient high pressure in human adipose microvessels.
MedLine Citation:
PMID:  24778165     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Increased intraluminal pressure can reduce endothelial function in resistance arterioles; however, the mechanism of this impairment is unknown. The purpose of this study was to determine the effect of local renin-angiotensin system inhibition on the pressure-induced blunting of endothelium-dependent vasodilation in human adipose arterioles. Arterioles (100-200 μm) were dissected from fresh adipose surgical specimens, cannulated onto glass micropipettes, pressurized to an intraluminal pressure of 60 mmHg, and constricted with endothelin-1. Vasodilation to ACh was assessed at 60 mmHg and again after a 30-min exposure to an intraluminal pressure of 150 mmHg. The vasodilator response to ACh was significantly reduced in vessels exposed to 150 mmHg. Exposure of the vessels to the superoxide scavenger polyethylene glycol-SOD (100 U/ml), the ANG II type 1 receptor antagonist losartan (10(-6) mol/l), or the angiotensin-converting enzyme inhibitor captopril (10(-5) mol/l) prevented the pressure-induced reduction in ACh-dependent vasodilation observed in untreated vessels. High intraluminal pressure had no effect on papaverine-induced vasodilation or ANG II sensitivity. Increased intraluminal pressure increased dihydroethidium fluorescence in cannulated vessels, which could be prevented by polyethylene glycol-SOD or losartan treatment and endothelial denudation. These data indicate that high intraluminal pressure can increase vascular superoxide and reduce nitric oxide-mediated vasodilation via activation of the vascular renin-angiotensin system. This study provides evidence showing that the local renin-angiotensin system in the human microvasculature may be pressure sensitive and contribute to endothelial dysfunction after acute bouts of hypertension.
Authors:
Matthew J Durand; Shane A Phillips; Michael E Widlansky; Mary F Otterson; David D Gutterman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  307     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2014 Jul 
Date Detail:
Created Date:  2014-08-11     Completed Date:  2014-08-27     Revised Date:  2014-10-22    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H25-32     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Adipose Tissue / blood supply,  physiology*
Arterioles / physiology*
Blood Flow Velocity / physiology
Blood Pressure / physiology
Female
Humans
Male
Microcirculation / physiology*
Middle Aged
Nitric Oxide / metabolism*
Renin-Angiotensin System / physiology*
Superoxides / metabolism*
Vasodilation / physiology*
Grant Support
ID/Acronym/Agency:
K23-HL-85614/HL/NHLBI NIH HHS; R01 HL094971/HL/NHLBI NIH HHS; R01 HL113612/HL/NHLBI NIH HHS; R01-HL-094971/HL/NHLBI NIH HHS; R01-HL-113612/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
11062-77-4/Superoxides; 31C4KY9ESH/Nitric Oxide

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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