Does calcium mediate the increase in potassium permeability due to phenylephrine or angiotensin II in the liver?

SJ Weiss and JW Putney

Two agonists, phenylephrine and angiotensin II, which have been shown to alter K+ permeability in the liver were investigated as to the possible role of Ca++ in the K+ release response (measured as 86Rb efflux) in liver slices. Both phenylephrine and angiotensin II caused transient increases in 86Rb efflux from liver slices. For both agonists, the first in a series of responses was independent of extracellular Ca++, but Ca++ was required to obtain a subsequent response. This dependence on extracellular Ca++ for a second response was not receptor-specific suggesting that activation of either receptor elicited the release of the same cellular pool of Ca++. The cationophore, A-23187, only slightly increased 45Ca++ efflux and was without effect on 86Rb efflux. In contrast to the ionophore, phenylephrine stimulated a precipitous rise in 45Ca++ efflux. It is proposed that the liver may be similar to a number of other tissues in that Ca++ mediates changes in K+ permeability, but that the source is a bound Ca++ store, rather than the extracellular space.

Volume 207, Issue 3, pp. 669-676, 12/01/1978
Copyright © 1978 by American Society for Pharmacology and Experimental Therapeutics