It is well established that taurine deficiency is associated with myocardial contractile dysfunction; however, the mechanism is unknown. As a follow-up to finding reduced force generation in taurine-depleted rat cardiac trabeculae, using either calcium or strontium activation, this study examined alterations in ventricular fine structure and contractile proteins in animals made taurine deficient by in vivo treatment with a taurine transport antagonist, guanidinoethane sulfonate. Observations of ventricular ultrastructure showed disordered contractile filaments and clear losses of myofibrillar bundles in association with taurine deficiency. Biochemical analyses of ventricular contractile proteins using polyacrylamide gel electrophoresis confirmed losses of the major sarcomeric proteins, myosin and actin. These findings provide a possible mechanism for the contractile deficits and cardiomyopathy described in taurine-deficient animals.
- Copyright © 1993 the American Physiological Society