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Excess of Glucocorticoid Induces Cardiac Dysfunction via Activating Angiotensin II Pathway

IR@IICB: CSIR-Indian Institute of Chemical Biology, Kolkata

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Title Excess of Glucocorticoid Induces Cardiac Dysfunction via Activating Angiotensin II Pathway
 
Creator Ghose Roy, Sreerupa
De, Priyanka
Mukherjee, Debasri
Chander, Vivek
Konar, Aditya
Bandyopadhyay, Debasish
Bandyopadhyay, Arun
 
Subject Cell Biology & Physiology
 
Description Background: Glucocorticoid is widely used as an anti-inflammatory drug in various diseases however excess of it often causes cardiovascular complications. The present study was undertaken to understand the molecular mechanism of glucocorticoid-induced cardiac dysfunction. Methods: Rats were treated daily with synthetic glucocorticoid, dexamethasone with or without mifepristone or losartan up to 15 days. Hemodynamic parameters were measured by PV-loop method using Millar’s instrument. Cardiac remodelling, fibrosis and oxidative stress were monitored after 15 days. Results: The systolic blood pressure was increased whereas the heart beat and cardiac output (n=6) were decreased by dexamethasone. Dexamethasone caused increase in the heart weight to body weight ratio (P<0.001, n=20), increased level of mRNA of atrial natriuretic peptide and an increased deposition of collagens in the extracellular matrix of the left ventricle which were inhibited by both mifepristone and losartan. The rate of oxygen consumption was decreased in association with increased levels of hypoxia inducible factor 1
 
Publisher Karger
 
Date 2009
 
Type Article
PeerReviewed
 
Format application/pdf
 
Identifier http://www.eprints.iicb.res.in/258/1/CELLULAR_PHYSIOLOGY_AND_BIOCHEMISTRY%2C_24(1%2D2)%2C1%2D10%2C2009[131].pdf
Ghose Roy, Sreerupa and De, Priyanka and Mukherjee, Debasri and Chander, Vivek and Konar, Aditya and Bandyopadhyay, Debasish and Bandyopadhyay, Arun (2009) Excess of Glucocorticoid Induces Cardiac Dysfunction via Activating Angiotensin II Pathway. Cellular Physiology and Biochemistry, 24 (1-2). 01-10.
 
Relation http://dx.doi.org/10.1159/000227803
http://www.eprints.iicb.res.in/258/