Mobilization of hepatic calcium pools by platelet activating factor

In the perfused rat liver, platelet activating factor, 1-O-hexadecyl-2-acetyl-sn-glycero-3-phosphocholine (AGEPC), infusion produces an extensive but transient glycogenolytic response which at low AGEPC concentrations (i.e., 10(-11) M) is markedly dependent upon the perfusate calcium levels. The role of calcium in the glycogenolytic response of the liver to AGEPC was investigated by assessing the effect of AGEPC on various calcium pools in the intact liver. Livers from fed rats were equilibrated with 45Ca2+, and the kinetics of 45Ca2+ efflux were determined in control, AGEPC-stimulated, and phenylephrine-stimulated livers during steady-state washout of 45Ca2+. AGEPC treatment had only a slight if any effect on the pattern of steady-state calcium efflux from the liver, as opposed to major perturbations in the pattern of calcium efflux effected by the alpha-adrenergic agonist phenylephrine. Infusion of short pulses of AGEPC during the washout of 45Ca2+ from labeled livers caused a transient release of 45Ca2+ which was not abolished at low calcium concentrations in the perfusate. Moreover, there occurred no appreciable increase in the total calcium content in the liver perfusate at either high or low concentrations of calcium in the perfusion fluid. Infusion of latex beads, which are removed by the reticuloendothelial cells, caused the release of hepatic 45Ca2+ in a fashion similar to the case with AGEPC. Our findings indicate that AGEPC does not perturb a major pool of calcium within the liver as occurs upon alpha-adrenergic stimulation; it is likely that AGEPC mobilizes calcium from a smaller yet very important pool, very possibly from nonparenchymal cells in the liver.