On participation of the autonomic nervous system in the mechanisms of chemical carcinogenesis.

With the view of studying the role of autonomic nervous system in chemical carcinogenesis mechanism in outbred white male rats, chronically treated with NDEA, there has been investigated the modifying effect of some neurotropic pharmacological drugs which cause either stimulation or inhibition of: 1. adrenergic processes (noradrenalin, isoproterenol, clonidine, pyrroxane and propranolol); 2. cholinergic processes (proserine and atropine); 3. the function of the central nervous system (CNS)--caffeine and ethanol. Pharmacological activation of alpha-adrenoreceptors or blocking of both beta-adrenoreceptors and cholinoreceptors has been revealed to stimulate hepatocarcinogenesis. On the contrary, the administration of alpha-adrenoreceptors antagonist or beta-adrenoreceptor and cholinoreceptors agonists inhibited the process of carcinogenic transformation. Caffeine, being the CNS stimulator, has significantly promoted carcinogenesis, while ethanol has practically prevented NDEA effect. Clonidine has also demonstrated its anticarcinogenic action. The obtained data are being discussed in connection with chemical carcinogenesis influence upon the CNS integrative function in control and regulation of tissue homeostasis.