Effect of epinephrine on permeability to sugar and on the production of free glucose in skeletal muscle.

Epinephrine increases the permeability of isolated frog sartorius muscles to 3-O-methyl-~-glucose. This effect resembles the action of insulin in that, at 19’, there is an absolute lag of 30 min preceding a rise in permeability, while at 0” no alteration of permeability is seen during several hours of incubation. The delayed effect of epinephrine on permeability contrasts with its prompt glycogenolytic effect at 19”; the hormone also causes a distinct rise in the concentration of glucose 6-phosphate at 0”. The effect of epinephrine on permeability can be prevented completely by the addition of pronethalol, an adrenergic p-receptor blocking agent, to the medium. Moreover, when muscles that have been incubated with epinephrine are subsequently incubated with pronethalol, the hormonal effect on permeability is readily reversed. Adrenochrome does not affect permeability of sartorius muscles to sugar. Of the concentrations of epinephrine tested, the lowest one that causes a change in permeability is lo-? M. A supramaximal concentration, 10m5 M, produces an increase in permeability that is equivalent to that of a submaximal concentration of insulin, 50 punits per ml. The effects of supramaximal concentrations of epinephrine and insulin on permeability are not additive; thus, the two hormones appear to act on the same transport system for sugar. However, epinephrine causes the formation of free glucose within the cells, and this glucose in turn induces counterflow transport when the movement of 3-O-methyl-Dglucose across the cell membrane is studied. The fact that epinephrine accelerates the formation of free glucose in muscle cells should be taken into consideration when the effects of epinephrine on utilization of sugars in muscle are evaluated.