Early changes in excitation-contraction coupling: transition from compensated hypertrophy to failure in Dahl salt-sensitive rat myocytes

Abstract

Our results indicated that: (I) normal Ca2+ homeostasis is preserved at the stage of compensated hypertrophy; (2) the early signs of isolated myocyte dysfunction were a prolongation of the shortening and relaxation time course without an abnormal time course of the Ca2+ transient. Thus, in the hypertensive Dahl salt rat model, abnormal Ca2+ handling appears neither to precede nor initiate the transition to failure.