Document Detail


Reversal of experimental renovascular hypertension restores coronary microvascular function and architecture.
MedLine Citation:
PMID:  21233798     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Hypertension (HTN) may lead to left ventricular hypertrophy and vascular dysfunction, which are independent factors for adverse cardiovascular outcomes. We hypothesized that decreased blood pressure by percutaneous transluminal renal angioplasty (PTRA) would improve the function and architecture of coronary microvessels, in association with decreased inflammation and fibrosis.
METHODS: Three groups of pigs were studied: normal, HTN, and HTN+PTRA. After 6 weeks of renovascular HTN, induced by placing a local-irritant coil in the renal artery, pigs underwent PTRA or sham. Four weeks later multidetector-computed tomography (CT) was used to assess systolic, diastolic, and microvascular function, and responses to adenosine. Microvascular architecture, oxygen sensors, inflammation, and fibrosis were then explored in cardiac tissue.
RESULTS: PTRA successfully decreased blood pressure and left ventricular hypertrophy. Basal fractional vascular volume (FVV) was similar among the groups, but its response to adenosine was significantly attenuated in HTN, whereas microvascular permeability (MP) and response to adenosine were greater than normal. Both were restored by PTRA. These were accompanied by increased myocardial expression of hypoxia-inducible factor (HIF)-1α, inflammation, and microvascular remodeling, including increased density of epicardial microvessels (20-200 µm), as well as cardiac diastolic dysfunction, all of which improved by reversal of HTN. However, PTRA only partially decreased myocardial fibrosis.
CONCLUSIONS: Reversal of early renovascular HTN improved coronary microvascular function and architecture and reversed myocardial hypertrophy and diastolic dysfunction, in association with decreased levels of myocardial ischemia and inflammation markers, underscoring the benefits of blood pressure normalization for preservation of cardiovascular function and structure.
Authors:
Victor H Urbieta-Caceres; Xiang-Yang Zhu; Matthew E Gibson; Frederic D Favreau; Kyra Jordan; Amir Lerman; Lilach O Lerman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-01-13
Journal Detail:
Title:  American journal of hypertension     Volume:  24     ISSN:  1941-7225     ISO Abbreviation:  Am. J. Hypertens.     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-22     Completed Date:  2011-07-01     Revised Date:  2014-09-21    
Medline Journal Info:
Nlm Unique ID:  8803676     Medline TA:  Am J Hypertens     Country:  United States    
Other Details:
Languages:  eng     Pagination:  458-65     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Angioplasty
Animals
Capillary Permeability
Female
Hypertension, Renovascular / physiopathology*,  therapy
Hypertrophy, Left Ventricular / physiopathology,  prevention & control
Hypoxia-Inducible Factor 1, alpha Subunit / biosynthesis
Kidney / blood supply
Microvessels / pathology,  physiology*
Procollagen-Proline Dioxygenase / biosynthesis
Renal Artery Obstruction / physiopathology
Swine
Von Hippel-Lindau Tumor Suppressor Protein / biosynthesis
Grant Support
ID/Acronym/Agency:
DK73013/DK/NIDDK NIH HHS; DK73608/DK/NIDDK NIH HHS; HL085307/HL/NHLBI NIH HHS; HL77131/HL/NHLBI NIH HHS; P01 HL085307/HL/NHLBI NIH HHS; P01 HL085307-04/HL/NHLBI NIH HHS; R01 DK073608/DK/NIDDK NIH HHS; R01 DK073608-05/DK/NIDDK NIH HHS; R01 HL077131/HL/NHLBI NIH HHS; R01 HL077131-06/HL/NHLBI NIH HHS; R21 DK077013/DK/NIDDK NIH HHS; R21 DK077013-01A2/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Hypoxia-Inducible Factor 1, alpha Subunit; EC 1.14.11.2/Procollagen-Proline Dioxygenase; EC 6.3.2.19/Von Hippel-Lindau Tumor Suppressor Protein
Comments/Corrections
Comment In:
Am J Hypertens. 2011 Apr;24(4):381-2   [PMID:  21423133 ]

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


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