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

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.