Sugar transport regulation in avian red blood cells: role of Ca2+ in the stimulatory effects of anoxia, adrenaline, and ascorbic acid.

Membrane transport of sugar and Ca2+ was studied in pigeon erythrocytes by measuring the cell to medium distribution of 3-O-[14C]methyl-D-glucose and 45Ca. We have found that stimulation of sugar transport by anoxia, adrenaline, or ascorbic acid was not dependent on external Ca2+, nor was it additive to the stimulatory effect of the calcium ionophore A23187. Stimulation by ascorbic acid was dependent on concentration and time. The slow basal 45Ca efflux was greatly accelerated by A23187, and this was further increased by adrenaline. A metabolic substrate mixture consisting of adenine, inosine, and fumarate (AIF) did not alter 45Ca efflux, except for antagonizing the effect of adrenaline in the presence of A23187. Sugar transport, whether basal or stimulated by adrenaline or ascorbic acid, was significantly decreased by AIF, independently of external Ca2+. Stimulation by A23187 in the absence of external Ca2+ was also antagonized by AIF. In cells depleted of Ca2+ by treatment with A23187 and EGTA, transport stimulation by adrenaline was abolished. These results suggest that release of Ca2+ from intracellular storage into the cytoplasm plays a role in the stimulation of sugar transport by adrenaline and anoxia and also by A23187 in the absence of external Ca2+. The data provide further indirect support for a calcium-dependent mechanism of sugar transport regulation in nucleated erythrocytes.