1977 Volume 18 Issue 6 Pages 860-866
The effects of epinephrine (1×10-6-1×10-5M) on the resting membrane potential and the K+-activated hyperpolarization of bullfrog atrial heart muscles were studied by the single sucrose-gap method or by intracellular microelectrode filled with 3M KCl. Epinephrine-induced hyperpolarization (Ep-hyperpolarization) was completely eliminated by the effect of ouabain or by removal of extracellular K+. The amplitude of K+-activated hyperpolarization, which was produced when the extracellular K+ concentration was raised from zero to 2mM, was markedly increased in the presence of epinephrine. The membrane depolarizations, due to high extracellular K+ concentration in the presence of ouabain (5×10-6M) which completely and reversibly eliminated the K+-activated hyperpolarization, were not altered under the effect of epinephrine.
These results suggested that Ep-hyperpolarization of bullfrog atrial heart muscles was due to the acceleration of electrogenic Na+ pump which produced the K+-activated hyperpolarization.
