The interaction of ethanol with central histaminergic stimulation of the pituitary-adrenocortical and hyperlipemic activity.

Ethanol introduced intragastrically (i.g.) in rats increased the pituitary-adrenocortical activity, measured indirectly through corticosterone concentration in blood serum. Since this increase reached only about 40% of the maximum hormone levels observed in that species after another stimuli, ethanol may be considered as a relatively weak stimulus. Ethanol induced also a significant decrease in serum free fatty acid (FFA) levels which was blocked totally by a prior intracerebroventricular (i.c.v.) administration of either H1- or H2-histamine receptor antagonists, mepyramine or metiamide and cimetidine. The ethanol-induced increase in serum corticosterone was insensitive to a central histamine H1- and H2-receptors blockade. Ethanol abolished the rise in serum FFA levels induced by an i.c.v. administration of histamine, pyridylethylamine (PEA)-a H1-receptor agonist, and dimaprit--a H2-receptor agonist. The histamine- and histamine-agonists induced increases of serum corticosterone were generally slightly intensified by a prior i.g. administration of ethanol.