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.
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