Glucagon and vasopressin interactions on Ca2+ movements in isolated hepatocytes

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Abstract
The effects of glucagon and vasopressin, singly or together, on cytosolic free Ca2+ concentration ([Ca2+]i) and on the 45Ca2+ efflux were studied in isolated rat liver cells. (1) In the presence of 1 mM external Ca2+, glucagon and vasopressin added singly induced sustained increases in [Ca2+]i. The rate of the initial fast phase of the [Ca2+]i increase and the magnitude of the final plateau were dependent on the concentrations (50 pM-0.1 .mu.M) of glucagon and vasopressin. Preincubating the cells with a low concentration of glucagon (0.1 nM) for 2 min markedly accelerated the fast phase and elevated the plateau of the [Ca2+]i increase caused by vasopressin. (2) In the absence of external free Ca2+, glucagon and vasopressin transiently increased [Ca2+]i and stimulated the 45Ca2+ efflux from the cells, indicating mobilization of Ca2+ from internal store(s). Preincubating the cells with 0.1 nM-glucagon accelerated the rate of the fast phase of the [Ca2+]i rise caused by the subsequent addition of vasopressin. However, unlike what was observed in the presence of 1 mM-Ca2+, glucagon no longer enhanced the maximal [Ca2+]i response to vasopressin. (3) In the absence of external free Ca2+, higher concentrations (1 nM-0.1 .mu.M) of glucagon, which initiated larger increases in [Ca2+]i, drastically decreased the subsequent Ca2+ response to vasopressin (10 nM). At these concentrations, glucagon also decreased the vasopressin-stimulated 45Ca2+ efflux from the cells. It is suggested that, in the liver, glucagon accelerates the fast phase and elevates the plateau of the vasopressin-mediated [Ca2+]i increase respectively by (a) releasing Ca2+ from the same internal store as that permeabilized by vasopressin, probably the endoplasmic reticulum, and (2) potentiating the influx of extracellular Ca2+ caused by this hormone.