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.
D000804:Angiotensin II / Q000494:pharmacology*; D000818:Animals; D000001:Calcimycin / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002463:Cell Membrane Permeability / Q000187:drug effects; D004347:Drug Interactions; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D010656:Phenylephrine / Q000494:pharmacology*; D011188:Potassium / Q000378:metabolism*; D011868:Radioisotopes; D012413:Rubidium
D011868:Radioisotopes; D000804:Angiotensin II; D010656:Phenylephrine; D000001:Calcimycin; D012413:Rubidium; D011188:Potassium; D002118:Calcium