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.
D000818:Animals; D001826:Body Fluids / Q000378:metabolism*; D002536:Cerebral Arteries / Q000378:metabolism*; D004285:Dogs; D005260:Female; D006947:Hyperkalemia / Q000378:metabolism; D007424:Intracellular Fluid / Q000378:metabolism*; D008297:Male; D010179:Pancreas / Q000502:physiology; D010180:Pancreatectomy; D011188:Potassium / Q000008:administration & dosage / Q000378:metabolism*; D014513:Ureter / Q000502:physiology
D011188:Potassium