5-(N,N-dimethyl)amiloride-sensitive Na-Li exchange in isolated specimens of human atrium.

H H Rasmussen; R D Harvey; E J Cragoe; R E ten Eick

doi:10.1172/JCI113740

Reingold ECG Center, Northwestern University, Chicago, Illinois 60611.

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Reingold ECG Center, Northwestern University, Chicago, Illinois 60611.

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Reingold ECG Center, Northwestern University, Chicago, Illinois 60611.

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Reingold ECG Center, Northwestern University, Chicago, Illinois 60611.

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Published in Volume 82, Issue 4 on October 1, 1988
J Clin Invest. 1988;82(4):1366–1375. https://doi.org/10.1172/JCI113740.
© 1988 The American Society for Clinical Investigation

Published October 1, 1988 - Version history

To examine if a transmembrane Na-Li exchange similar to that reported to occur in human blood cells can be demonstrated in the heart, we incubated specimens of human atrium in cold (2-3 degrees C) Li-Tyrode's solution. The Li-loaded, Na-depleted specimens were then transferred to warm (30 degrees C) Na-Tyrode's solution. After transfer the membrane potential hyperpolarized to a level more negative than the equilibrium potential for K+. The hyperpolarization was inhibited by acetylstrophanthidin or K+-free solution indicating that it was due to current produced by the Na, K-pump responding to a Na load. This suggested that intracellular Li+ had been exchanged for Na+. The hyperpolarization was abolished by 10 microM 5-(N,N-dimethyl)amiloride while 10 microM bumetanide had no effect, findings that are consistent with the notion that the exchange of intracellular Li+ for extracellular Na+ occurs via an operational mode of the Na-H exchanger rather than being mediated through a mechanism involving the Na/K/2Cl cotransporter.