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Cyclic AMP and Aclrenergic Receptor Control of Rat Liver Glycogen Metabolism

Section on Physiological Controls, Laboratory of Biomedical Sciences, National Institute of Child Health and Human Development NIH, Bethesda, Maryland 20014

Abstract

We used the isolated perfused rat liver as a model system to study mechanisms by which catecholamines alter hepatic carbohydrate metabolism. Epinephrine, norepinephrine, phenylephrine and isoproterenol all cause activation of glycogen phosphorylase, and increase glucose output. The effects of all of these agents are blocked by the alpha blocker phentolamine, whereas the beta blocker propranolol only inhibits the effect of norepinephrine. Cyclic AMP levels rise in the liver and the perfusate following epinephrine. This rise is accentuated by phentolamine and blocked by propranolol. Isoproterenol causes a greater elevation of cyclic AMP than phenylephrine while the reverse is true with respect to phosphorylase. The above data leads us to conclude that there are two independent mechanisms whereby catecholamines may activate glycogenolysis: 1) a beta receptor—mediated effect resulting in a rise in cellular cyclic AMP levels, which by the wellknown cascade mechanism activates phosphorylase; and 2) an alpha receptor—mediated effect which occurs by a cyclic AMP—independent mechanism; possibly involving hypoxemia secondary to vasoconstriction.

In addition, there probably exists on the hepatic parenchymal cell a separate set of alpha receptors which inhibit the rise in cyclic AMP consequent to beta receptor stimulation. (Endocrinology 91: 680, 1972)

Received July 6, 1971.

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