Effects of epinephrine on resting potential in normal and hypertrophied cardiac muscles

The role of the Na-K pump in the control of cellular ion balance has long been appreciated. Recent studies suggest that the manner in which this ion transport system functions in hypertrophied failing (HF) cardiac muscle is markedly different from that seen in normal muscles. The ability of the sympathetic neurohormone, epinephrine, to modulate membrane potential changes thought to reflect the activity of the Na-K pump in normal and HF cardiac muscle was examined in this study. Specifically rate-related changes in membrane potential (Emax) thought to be associated with the Na-K pump were measured in intact functioning cat papillary muscles. The results of these studies demonstrate that the rate-related changes in Emax thought to be associated with Na-K activity were markedly altered in HF cardiac muscles. Emax in these muscles responded to periods of transient stimulation by first depolarizing and then slowly returning to a new steady state which was depolarized with respect to the initial predrive Emax. Emax in normal muscles also depolarized on drive, but returned to a new steady state more rapidly and eventually hyperpolarized. Epinephrine significantly affected these rate-related changes in Emax in normal muscles by causing all the rates of change in Emax to be increased. In HF muscles, on the other hand, epinephrine had no significant effect on these parameters at the concentration tested. These results suggest that under certain conditions HF cardiac muscle may be incapable of maintaining normal resting membrane potentials. In addition the modulating influence of epinephrine is markedly blunted.