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AngII-induced compensatory hypertrophy is associated with unaltered substrate utilization and
efficiency in murine hearts
Pedersen TM1, Aasum E1 and Hafstad AD1
1Cardiovascular
Research Group, Department of Medical Biology, Faculty of Health Sciences, UiT The Arctic University of Norway, Tromsø, Norway
Introduction. Altered cardiac metabolism and impaired energetics has been implicated in the
development of heart failure. The role of Angiotensin II (AngII) is well established in the pathogenesis
and progression of heart failure, but less is known about how lower doses of AngII affect the heart’s
metabolism and oxygen utilization. In this study we wanted to investigate how a slow-pressor dose
affects cardiac metabolism and oxygen consumption prior to the development of ventricular
dysfunction.
Materials and methods. C57BL/6J mice were treated (2 wk) with saline (sham) or AngII (400
ng/kg/min) using micro-osmotic pumps. Blood pressures were measured (tail cuffs) and
echocardiography was done before and after treatment. Cardiac function, myocardial substrate
utilization and oxygen consumption was measured in isolated perfused hearts.
Results. AngII treatment led to a slight reduction in body weight gain, while there was no measurable
effect on blood pressure. Echocardiographic measurements revealed a significant increase in ejection
fraction, fractional shortening and left ventricle wall thickness in AngII treated mice. The increased
heart weight (10%) also confirmed cardiac hypertrophy. Isolated hearts from AngII mice exhibited a
higher heart rate, while cardiac output was unaltered. AngII treatment did not alter glucose or fatty acid
oxidation rates, nor did it alter oxygen consumption or mechanical efficiency.
Conclusion. This slow-pressor dose of AngII induced a compensated hypertrophy with unaltered
cardiac efficiency and substrate utilization in murine hearts.