Intracellular potassium activity in guinea pig papillary muscle during prolonged hypoxia.

1982 
During prolonged hypoxia, intracellular potassium concentration, [K]i has been reported to fall by 70% with a concomitant decrease in the calculated potassium equilibrium potential, EK. Nevertheless, resting membrane potential, Vm, declined only slightly. Because Vm depolarized very little in relation to the calculated EK, it was hypothesized that electrogenic Na-K pumping contributed up to 40 mV to Vm during prolonged hypoxia. To further test this hypothesis we studied what changes prolonged hypoxia makes in the thermodynamically active fraction of cellular potassium, intracellular potassium activity, αKi, and how change in αKi affects the relationship between Vm, EK and, by inference, the Na-K pump. Using double-barrel K-selective electrodes, Vm and αKi were measured in quiescent guinea pig right ventricular papillary muscles superfused for 8 h with hypoxic Tyrode's solution. Over the 8-h period both Vm and αKi decreased. However, the decline in Vm was paralleled by a decrease in the EK calculated from αKi. At no time was there hyperpolarization of Vm beyond EK. After 8 h the Na-K pump was inhibited by exposing the muscles to 0.1 mM ouabain. The onset of an increase in extracellular potassium activity, measured with a double-barrel electrode, was used to mark the amount of depolarization of Vm due solely to pump inhibition. After hypoxia, Vm depolarized 8.4±4.4 mV before extracellular potassium activity (αKe) increased. Thus, the decrease in αKi during hypoxia is much less than that reported for [K]i. The parallel decline in Vm and EK and the small depolarization of Vm with ouabain suggest that after prolonged hypoxia the Na-K pump continues to contribute to Vm, but the amount of this contribution is substantially less than previously reported.
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