Enhancement of K transfer to intracellular fluid by cerebral artery K-loading.

Intact, UL, and pancreatectomized UL dogs were loaded with K by administration of 2 mEq KCl/kg/hr through a cerebral (vertebral) artery. K transfer to ICF was calculated and compared with that computed in control animals K-loaded through a PV. At the same rate of K administration, the change of route from PV to VA markedly increased transmembrane K transfer, even in the absence of insulin; the increase seems a specific response to K. KCl administration via a VA, with a resulting abrupt rise in the serum K concentration of cerebral blood, activates a K transfer mechanism (possibly by stimulation of a K-sensitive CNS receptor) that is strikingly unlike the insulin-mediated one stimulated by intravenous KCl. Hyperkalemic dogs may have more than one mechanism for maintaining K homeostasis, depending on the rate at which K enters the circulation.