No abstract

The short-term effects of vasopressin on free fatty acids and lysophospholipids were investigated in hepatocytes isolated from fed rats. Over the time period 0.25 to 10 min vasopressin decreased the steady-state concentrations of palmitic, stearic and oleic acids measured by gas liquid chromatography in extracts of cells incubated at 0.1 mM extracellular Ca2+. The concentrations of arachidonic and linoleic acids did not change. In hepatocytes labelled with [3H]arachidonic acid and incubated at 1.3 mM extracellular Ca2+ vasopressin or the Ca2+-selective ionophore A23187 increased the rate of accumulation of radioactivity in the incubation medium by 40%. The action of A23187 was dependent on extracellular Ca2+. When hepatocytes labelled with 32Pi were treated with vasopressin, no change in the amounts of [32P]lysophosphatidylethanolamine or [32P]lysophosphatidylcholine was observed. It is concluded that the action of vasopressin on hepatocytes is associated with the release of arachidonic acid or metabolites of arachidonic acid but is not accompanied by a general increase in the steady-state concentrations of free fatty acids and lysophospholipids.

Exposure of isolated hepatocytes to glucagon for 45 min caused a 2.5-fold increase in the time (Ca2+ retention time) for which mitochondria subsequently isolated from the cells retained a load of exogenous Ca2+ before its spontaneous release. Half maximal effect of glucagon was observed at a concentration of 0.6 nM. An increase in the Ca2+ retention time was observed after 30 but not 15 min exposure of cells to the hormone. Incubation of hepatocytes with dexamethasone, epinephrine, vasopressin, dibutyryl cyclic AMP or 8-bromo cyclic GMP also induced an increase in mitochondrial Ca2+ retention time. The effect of glucagon was associated with an increase in cellular cyclic AMP and was inhibited by puromycin, cycloheximide and cordycepin, but not by actinomycin D or chloramphenicol. Puromycin caused only a small inhibition of the stimulation by glucagon of mitochondrial pyruvate carboxylation. It is concluded that the effects of glucagon on mitochondrial Ca2+ retention require nuclear DNA-directed protein synthesis and differ, in this respect, from the rapid-onset effects of the hormone on other mitochondrial properties, including pyruvate carboxylation.