[Lack of beta-adrenergic stimulation of membrane bound adenyl cyclase in psoriasis as compared to normal epidermis (author's transl)].
Glucagon and beta-adrenergic compounds such as 1-isoproterenol stimulated the low activity of an ATP-utilizing enzyme located on the cell membranes of normal keratinocytes. Addition of beta-antagonist propranolol to the incubation medium prevented the stimulatory effect of 1-isoproterenol. We considered, therefore, the reaction product being due to epidermal membrane-bound adenyl cyclase activity. In psoriatic epidermis the basal adenyl cyclase activity was low, similar to normal epidermis, however, glucagon and 1-isoproterenol failed to stimulate the enzyme activity in psoriasis under the same conditions. It seems, therefore, that the beta-adrenergic-cAMP cascade as a regulatory epidermal control mechanism of induced proliferation is ineffective in this disease.
D000262:Adenylyl Cyclases / Q000378:metabolism*; D002462:Cell Membrane / Q000201:enzymology; D004789:Enzyme Activation; D005934:Glucagon / Q000494:pharmacology; D006801:Humans; D066298:In Vitro Techniques; D007545:Isoproterenol / Q000037:antagonists & inhibitors / Q000494:pharmacology; D008544:Melanocytes / Q000201:enzymology; D011433:Propranolol / Q000494:pharmacology; D011565:Psoriasis / Q000201:enzymology*; D011941:Receptors, Adrenergic; D012867:Skin / Q000201:enzymology*
D011941:Receptors, Adrenergic; D005934:Glucagon; D011433:Propranolol; D000262:Adenylyl Cyclases; D007545:Isoproterenol
Beta-Adrenerge Stimulation membrangebundener Adenylcyklase in normaler Epidermis und mangelnde Stimulierbarkeit bei Psoriasis