[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.