Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/10513
Title: Acute kidney injury in the rat causes cardiac remodelling and increases angiotensin-converting enzyme 2 expression.
Austin Authors: Burchill, Luke J;Velkoska, Elena;Dean, Rachael G;Lew, R A;Smith, A I;Levidiotis, Vicki;Burrell, Louise M 
Affiliation: Department of Medicine, University of Melbourne, Austin Health, Heidelberg, Victoria 3081, Australia
Issue Date: 25-Jan-2008
Publication information: Experimental Physiology 2008; 93(5): 622-30
Abstract: Patients with kidney failure are at high risk of a cardiac death and frequently develop left ventricular hypertrophy (LVH). The mechanisms involved in the cardiac structural changes that occur in kidney failure are yet to be fully delineated. Angiotensin-converting enzyme (ACE) 2 is a newly described enzyme that is expressed in the heart and plays an important role in cardiac function. This study assessed whether ACE2 plays a role in the cardiac remodelling that occurs in experimental acute kidney injury (AKI). Sprague-Dawley rats had sham (control) or subtotal nephrectomy surgery (STNx). Control rats received vehicle (n = 10), and STNx rats received the ACE inhibitor (ACEi) ramipril, 1 mg kg(-1) day(-1) (n = 15) or vehicle (n = 13) orally for 10 days after surgery. Rats with AKI had polyuria (P < 0.001), proteinuria (P < 0.001) and hypertension (P < 0.001). Cardiac structural changes were present and characterized by LVH (P < 0.001), fibrosis (P < 0.001) and increased cardiac brain natriuretic peptide (BNP) mRNA (P < 0.01). These changes occurred in association with a significant increase in cardiac ACE2 gene expression (P < 0.01) and ACE2 activity (P < 0.05). Ramipril decreased blood pressure (P < 0.001), LVH (P < 0.001), fibrosis (P < 0.01) and BNP mRNA (P < 0.01). These changes occurred in association with inhibition of cardiac ACE (P < 0.05) and a reduction in cardiac ACE2 activity (P < 0.01). These data suggest that AKI, even at 10 days, promotes cardiac injury that is characterized by hypertrophy, fibrosis and increased cardiac ACE2. Angiotensin-converting enzyme 2, by promoting the production of the antifibrotic peptide angiotensin(1-7), may have a cardioprotective role in AKI, particularly since amelioration of adverse cardiac effects with ACE inhibition was associated with normalization of cardiac ACE2 activity.
Gov't Doc #: 18223026
URI: https://ahro.austin.org.au/austinjspui/handle/1/10513
DOI: 10.1113/expphysiol.2007.040386
Journal: Experimental physiology
URL: https://pubmed.ncbi.nlm.nih.gov/18223026
Type: Journal Article
Subjects: Acute Kidney Injury.enzymology.genetics.pathology
Angiotensin-Converting Enzyme Inhibitors.pharmacology
Animals
Autoradiography
Blood Pressure.physiology
Body Weight.drug effects
Collagen.metabolism
Drinking.physiology
Fluorescent Dyes
Gene Expression Regulation, Enzymologic.physiology
Heart Function Tests
Heart Rate.physiology
Kidney Function Tests
Myocardium.enzymology.pathology
Nephrectomy
Peptidyl-Dipeptidase A.biosynthesis
Proteinuria.etiology
RNA, Messenger.biosynthesis.genetics
Rats
Reverse Transcriptase Polymerase Chain Reaction
Urodynamics.physiology
Ventricular Remodeling.physiology
Appears in Collections:Journal articles

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