Echocardiography shows impaired cardiac function in ACE2 knockout mice

Abstract

<p>Background: Angiotensin converting enzyme2 (ACE2) is a monocarboxypeptidase that metabolizes the potent vasoconstrictor peptide, angiotensin II (Ang II), to the vasodilator Ang (1-7). Since ACE2 is thought to regulate heart function, we hypothesized that loss of ACE2 would negatively affect function and alter the response to Ang ILMethods: Echocardiographic (Echo) measurements were made in control and ACE2 knockout(KO) mice under baseline and Ang II stimulated conditions (1000 ng Ang II/kg/min for 4 weeks). Echos were recorded using a Siemens® ACUSON system. Images of the left ventricle were taken in the M-Mode and 2-D Mode. left ventricular end diastolic and end systolic areas as well as dimensions (lVEDa, lVESa, lVEDd, and lVESd) respectively, were measured. Ejection fraction (EF) was calculated. Posterior wall thickness (PWT) and septal wall thickness (SWT) were measured in the M-Mode. Results: Baseline Echo measurements show higher lVESa (~+10%) in ACE2KO vs Control. This corresponds to a decrease in EF (~-25%). Ang II infusion produced a marked increase in lVESa (~+19%) in ACE2KO mice as compared to controls (~+9%). This meant that there was a greater decrease in EF in KO mice (~-165%) vs controls (~-125%). There was no sign of dilated cardiomyopathy as shown by PWT and SWT measurements. Conclusion: Results suggest a protective role for ACE2 in the control of cardiac contractile function under baseline and Ang II stimulation.</p><p>This presentation occurred at the Wright State University Campus-Wide Celebration of Research, Scholarship and Creative Activities on April 8, 2011</p>