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Participation of the autonomic nervous system in the mechanisms of chemical carcinogenesis



Participation of the autonomic nervous system in the mechanisms of chemical carcinogenesis



Neoplasma 29(3): 301-308



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

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