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    Chronic kidney disease: cardiac and renal angiotensin-converting enzyme (ACE) 2 expression in rats after subtotal nephrectomy and the effect of ACE inhibition

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    Author
    Burrell, LM; Burchill, L; Dean, RG; Griggs, K; Patel, SK; Velkoska, E
    Date
    2012-04-01
    Source Title
    EXPERIMENTAL PHYSIOLOGY
    Publisher
    WILEY-BLACKWELL
    University of Melbourne Author/s
    Burrell, Louise; BURCHILL, LUKE; DEAN, RACHAEL; Griggs, Karen; Patel, Sheila; Velkoska, Elena; Burchill, Luke
    Affiliation
    Medicine - Austin Health
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Burrell, L. M., Burchill, L., Dean, R. G., Griggs, K., Patel, S. K. & Velkoska, E. (2012). Chronic kidney disease: cardiac and renal angiotensin-converting enzyme (ACE) 2 expression in rats after subtotal nephrectomy and the effect of ACE inhibition. EXPERIMENTAL PHYSIOLOGY, 97 (4), pp.477-485. https://doi.org/10.1113/expphysiol.2011.063156.
    Access Status
    Access this item via the Open Access location
    URI
    http://hdl.handle.net/11343/32599
    DOI
    10.1113/expphysiol.2011.063156
    Open Access URL
    https://physoc.onlinelibrary.wiley.com/doi/epdf/10.1113/expphysiol.2011.063156
    Description

    C1 - Journal Articles Refereed

    Abstract
    Renin-angiotensin system blockade slows but does not prevent the cardiovascular complications of chronic kidney disease (CKD). Angiotensin-converting enzyme (ACE) 2 is differentially regulated in acute kidney injury, with increased cardiac ACE2 but decreased kidney ACE2 levels. This study investigated the effect of long-term ACE inhibition on cardiac and renal ACE2 in rats with CKD induced by subtotal nephrectomy (STNx). Sprague-Dawley rats had sham (control) or STNx surgery. Control rats received vehicle (n = 9) and STNx rats ramipril (1 mg kg(-1) day(-1); n = 10) or vehicle (n = 10) for 28 days. Subtotal nephrectomy resulted in impaired creatinine clearance (P < 0.05), proteinuria (P < 0.05), renal fibrosis (P < 0.05) and reduced renal cortical ACE2 mRNA (P < 0.05) and activity (P < 0.05). In rats with CKD, ramipril improved creatinine clearance (P < 0.05) and was associated with an increase in cortical but not medullary ACE2 activity (P < 0.05). Compared with control rats, STNx rats were hypertensive (P < 0.01), with increased left ventricular end-diastolic pressure (LVEDP; P < 0.01), left ventricular hypertrophy (LVH; P < 0.05) and interstitial (P < 0.05) and perivascular fibrosis (P < 0.01). In rats with CKD, ramipril decreased blood pressure (P < 0.001) and reduced LVEDP (P < 0.01), LVH (P < 0.01) and perivascular fibrosis (P < 0.05) but did not significantly reduce interstitial fibrosis. There was no change in cardiac ACE2 in rats with CKD compared with control rats. In rats with CKD, ACE inhibition had major benefits to reduce blood pressure and cardiac hypertrophy and to improve creatinine clearance, but did not significantly impact on cardiac ACE2, cardiac interstitial fibrosis, renal fibrosis or proteinuria. Thus, in rats with CKD, renal ACE2 deficiency and lack of activation of cardiac ACE2 may contribute to the progression of cardiac and renal tissue injury. As long-term ACE inhibition only partly ameliorated the adverse cardio-renal effects of CKD, adjunctive therapies that lead to further increases in ACE2 activity may be needed to combat the cardio-renal complications of CKD.
    Keywords
    Cardiology (incl. Cardiovascular Diseases); Nephrology and Urology; Cardiovascular System and Diseases; Urogenital System and Disorders

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