Mitochondrial Oxidative Phosphorylation and Calcium Transport in Cardiac Hypertrophy due to Pressure Overload in Pigs

Abstract

By virtue of their ability to generate energy in the form of ATP, mitochondria are known to play an important role in the maintenance of cardiac function (1). In addition, heart mitochondria have a remarkable capacity to accumulate a large quantity of calcium and are generally considered to serve as calcium sink in the myocardium under a wide variety of pathological conditions (2,3). In fact, an increase in Ca²⁺ uptake and a depression in oxidative phosphorylation activity have been reported in heart mitochondria isolated from animals with chronic potassium deficiency (4) and early stages of bacterial ardiomyopathy (5). Similar observations were also made with mitochondria isolated from Ca²⁺-paradoxic hearts obtained after a successive perfusion with Ca²⁺-free medium and Ca²⁺ –containin medium (6,7). Although mitochondria from different types of failing hearts have been reported to show depressed Ca²⁺ uptake and energy production (5, 8–10), the functional significance of these change is not clear because similar results were also obtained upon prolonged ingestion of alcohol under which conditions cardiac contractile force was unaltered (11).

This work was supported by a grant from the Medical Research Council of Canada.