Akasu T, Ohta Y, Koketsu K
Jpn Heart J. 1977 Nov;18(6):860-6. doi: 10.1536/ihj.18.860.
The effects of epinephrine (1 X 10(-6)--1 X 10(-5) M) 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 3 M KC1. 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 2 mM, was markedly increased in the presence of epinephrine. The membrane depolarizations, due to high extracellular K+ concentration in the presence of ouabain (5 X 10(-6) M) 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.
采用单蔗糖间隙法或用充满3M氯化钾的细胞内微电极，研究了肾上腺素（1×10⁻⁶ - 1×10⁻⁵M）对牛蛙心房肌静息膜电位和钾激活超极化的影响。哇巴因的作用或去除细胞外钾可完全消除肾上腺素诱导的超极化（Ep-超极化）。当细胞外钾浓度从零提高到2mM时产生的钾激活超极化幅度，在有肾上腺素存在时显著增加。在哇巴因（5×10⁻⁶M）存在下，由于高细胞外钾浓度导致的膜去极化完全且可逆地消除了钾激活超极化，在肾上腺素作用下并未改变。这些结果表明，牛蛙心房肌的Ep-超极化是由于产生钾激活超极化的电生性钠泵加速所致。
