Document Detail


ACE2 improves right ventricular function in a pressure overload model.
MedLine Citation:
PMID:  21695173     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Right ventricular (RV) dysfunction is a complication of pulmonary hypertension and portends a poor prognosis. Pharmacological therapies targeting RV function in pulmonary hypertension may reduce symptoms, improve hemodynamics, and potentially increase survival. We hypothesize that recombinant human angiotensin-converting enzyme 2 (rhACE2) will improve RV function in a pressure overload model.
RESULTS: rhACE2 administered at 1.8 mg/kg/day improved RV systolic and diastolic function in pulmonary artery banded mice as measured by in vivo hemodynamics. Specifically, rhACE2 increased RV ejection fraction and decreased RV end diastolic pressure and diastolic time constant (p<0.05). In addition, rhACE2 decreased RV hypertrophy as measured by RV/LV+S ratio (p<0.05). There were no significant negative effects of rhACE2 administration on LV function. rhACE2 had no significant effect on fibrosis as measured by trichrome staining and collagen1α1 expression. In pulmonary artery banded mice, rhACE2 increased Mas receptor expression and normalized connexin 37 expression.
CONCLUSION: In a mouse RV load-stress model of early heart failure, rhACE2 diminished RV hypertrophy and improved RV systolic and diastolic function in association with a marker of intercellular communication. rhACE2 may be a novel treatment for RV failure.
Authors:
Jennifer A Johnson; James West; Karen B Maynard; Anna R Hemnes
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2011-06-10
Journal Detail:
Title:  PloS one     Volume:  6     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2011  
Date Detail:
Created Date:  2011-06-22     Completed Date:  2011-11-02     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e20828     Citation Subset:  IM    
Affiliation:
Division of Allergy, Pulmonary, and Critical Care Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America. jennifer.johnson.2@vanderbilt.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Diastole / drug effects
Disease Models, Animal
Fibrosis
Hemodynamics / drug effects
Humans
Hypertrophy, Right Ventricular / pathology,  physiopathology
Immunohistochemistry
Male
Mice
Mice, Inbred C57BL
Microvessels / drug effects,  pathology
Peptidyl-Dipeptidase A / administration & dosage,  metabolism*,  pharmacology
Pressure*
Recombinant Proteins / pharmacology
Signal Transduction / drug effects
Systole / drug effects
Ventricular Function, Right / drug effects,  physiology*
Grant Support
ID/Acronym/Agency:
KO8 HL093363/HL/NHLBI NIH HHS; R01 HL095797/HL/NHLBI NIH HHS; T32 HL094296/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Recombinant Proteins; EC 3.4.15.1/Peptidyl-Dipeptidase A; EC 3.4.17.-/angiotensin converting enzyme 2
Comments/Corrections

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


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