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

During prolonged hypoxia, intracellular potassium concentration, K has been reported to fall by 70% with a concomitant decrease in the calculated potassium equilibrium potential, E(K). Nevertheless, resting membrane potential, V(m), declined only slightly. Because V(m) depolarized very little in relation to the calculated E(K), it was hypothesized that electrogenic Na-K pumping contributed up to 40 mV to V(m) 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, alpha(K) (i), and how change in alpha(K) (i) affects the relationship between V(m), E(K) and, by inference, the Na-K pump. Using double-barrel K-selective electrodes, V(m) and alpha(K) (i) 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 V(m) and alpha(K) (i) decreased. However, the decline in V(m) was paralleled by a decrease in the E(K) calculated from alpha(K) (i). At no time was there hyperpolarization of V(m) beyond E(K). 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 V(m) due solely to pump inhibition. After hypoxia, V(m) depolarized 8.4+/-4.4 mV before extracellular potassium activity (alpha(K) (e)) increased. Thus, the decrease in alpha(K) (i) during hypoxia is much less than that reported for K. The parallel decline in V(m) and E(K) and the small depolarization of V(m) with ouabain suggest that after prolonged hypoxia the Na-K pump continues to contribute to V(m), but the amount of this contribution is substantially less than previously reported.