AJP - Heart and Circulatory Physiology, Vol 256, Issue 1 256-H264, Copyright © 1989 by American Physiological Society
Na+-dependent activation of Na+-K+ pump in human myocardium during recovery from acidosis
H. H. Rasmussen, E. J. Cragoe Jr and R. E. ten Eick
Reingold ECG Center, Northwestern University, Chicago, Illinois 60611.
In cardiac cells of some species, an intracellular Na+ load and enhanced
electrogenic Na+ pumping can develop during recovery from acidosis. We
examined whether this can also occur in human heart. Specimens of human
right atrial appendage were incubated in cold (2 degrees C)
NH4Cl-substituted (for NaCl) Tyrode solution and then transferred to warm
(30 degrees C) Na+-Tyrode solution containing 20 mM K+ to induce an
intracellular acid load. After transfer, resting membrane potential (Em)
transiently hyperpolarized to a maximal level (Emax) of -58.6 +/- 1.3 mV (n
= 8), a level significantly (P less than 0.001) more negative than the
equilibrium potential for K+. Decreasing K+ conductance with 0.5 mM Ba2+
increased Emax to -74.0 +/- 2.7 mV (n = 6, P less than 0.001), indicating
that the hyperpolarization was not due to efflux of NH+4 through K
channels. Acetylstrophanthidin (0.5 microM) reduced Emax to -37.5 +/- 3.1
mV (n = 5, P less than 0.001), indicating that an increased level of Na+-K+
pump activity was involved in the hyperpolarization. The Na+-K+
pump-induced hyperpolarization was abolished (Emax = -22.6 +/- 1.6 mV, n =
8, P less than 0.001) by 10 microM 5-(N,N-dimethyl)amiloride and, when the
extracellular Na+ concentration was reduced to 50 mM, by 50 mM Li+. These
findings suggest that Na+-H+ exchange can produce a Na+ load which then can
stimulate electrogenic Na+ pumping in human cardiac cells during recovery
from acidosis.
