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|Title:||Changes in cardiac angiotensin converting enzyme after myocardial infarction and hypertrophy in rats.||Austin Authors:||Johnston, Colin I;Mooser, V;Sun, Y;Fabris, Bruno||Affiliation:||Department of Medicine, University of Melbourne, Austin Hospital, Heidelberg, Victoria, Australia||Issue Date:||1-Feb-1991||Publication information:||Clinical and Experimental Pharmacology & Physiology; 18(2): 107-10||Abstract:||1. Cardiac angiotensin-converting enzyme (ACE) is localized in high concentration in cardiac valves, coronary vessels, right and left atrium and right and left ventricle. 2. Cardiac ACE is functionally active in converting angiotension I to angiotensin II. 3. The level of cardiac ACE measured by radioinhibitor binding or by quantitative in vitro autoradiography was greatly increased after experimental myocardial infarction in the rat. The increase was greatest in the fibrous scar tissue of the free left ventricular wall infarct, but there were also significant increases in the ACE concentration in the four chambers of the heart. 4. Treatment with enalapril for 4 weeks following coronary ligation inhibited cardiac ACE, including the high levels found in the scar in the left ventricular free wall. 5. There was a close relationship between the systolic blood pressure and left ventricular mass in several models of experimental hypertension, despite varying degrees of activation of the renin-angiotensin system. However no relationship between the degree of left ventricular hypertrophy and changes in cardiac ACE could be determined. 6. Inhibition of cardiac ACE may contribute to the beneficial effect of ACE inhibitors in cardiac hypertrophy and remodelling, and may play a part in the cardioprotective role of ACE inhibitor.||Gov't Doc #:||1850674||URI:||http://ahro.austin.org.au/austinjspui/handle/1/10616||URL:||https://pubmed.ncbi.nlm.nih.gov/1850674||Type:||Journal Article||Subjects:||Animals
Rats, Inbred Strains
|Appears in Collections:||Journal articles|
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