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    STUDIA BIOLOGIA - Issue no. 2 / 2001  

  Abstract:  The Antiglucocorticoid Effect of Propranolol. Hormone secretion by the hypothalamic-pituitary-adrenocortical (HPA) axis is modulated by multiple factors which include the circadian rhythm, various types of stresses and glucocorticoids. It is also well demonstrated that multiple stimulatory agents can independently affect the function of the HPA axis. These stimulatory agents include catecholamines (CA) which exert their effect through a highly specific -adrenergic receptor, vasopressin and the peptidic corticotropin-releasing hormone (CRH). Clinical and experimental data clearly demonstrate that synthetic topical corticosteroids widely used in human dermatology, beside their excellent local actions, exert adverse secondary systemic side effects, due to their percutaneous absorption capacity. Therefore, it is advisable that the topical use of these steroids for long-term therapy be limited. It is also recommended to find the proper conditions for improving the benefit/risk ratio between their local and systemic adverse side actions. Literature data have been reported that the short-term epicutaneous application of some halogenated or nonhalogenated topical dermocorticosteroids in white Wistar rats exert steroid-diabetogen secondary side effects, manifested by hyperglycemia, hepatic and thymic glucose overproduction, elevated serum lipids. All these metabolic disorders were accompanied by pancreatic islet damage, thymolysis and alteration of HPA axis structure and ultrastructure. Some of these endocrino-metabolic disorders, according to our recent observations, are reducible by in vivo -adrenoreceptor blockage with Propranolol. Starting from the above findings and from the important physiological roles of the glucocorticoids in young organisms, we investigated the HPA axis reactions in prepubertal rats, after a short-term epicutaneous treatment with Clobetasol-propionate-containing cream, applied alone or associated with Propranolol, the -adrenoreceptor blocking agent.  
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