Mechanisms involved in alpha-adrenergic effects of catecholamines on liver metabolism.
Recent results have indicated that alpha-adrenergic receptors are the major mediators of catecholamine actions on liver metabolism in several species. It is well-established that cAMP and cAMP-dependent protein kinase are not involved in hepatic alpha-adrenergic effects. This review presents evidence that alpha-adrenergic stimulation of glycogenolysis in rat liver involves the mobilization of Ca2+ ions from mitochondria and stimulation of phosphorylase kinase by the resulting increase in cytosolic Ca2+ concentration. Possible mechanisms by which activation of alpha-adrenergic receptors causes release of mitochondrial Ca2+ and affects other cell processes are discussed.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002395:Catecholamines / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism; D005943:Gluconeogenesis / Q000187:drug effects; D008099:Liver / Q000378:metabolism*; D008112:Liver Glycogen / Q000378:metabolism; D006005:Phosphorylases / Q000378:metabolism; D011773:Pyruvates / Q000378:metabolism; D051381:Rats; D011941:Receptors, Adrenergic / Q000187:drug effects*; D011942:Receptors, Adrenergic, alpha / Q000187:drug effects*
D002395:Catecholamines; D008112:Liver Glycogen; D011773:Pyruvates; D011941:Receptors, Adrenergic; D011942:Receptors, Adrenergic, alpha; D000242:Cyclic AMP; D006005:Phosphorylases; D002118:Calcium