A vagally mediated histaminergic component of food-related drinking in the rat.

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Abstract
Histamine elicited drinking in a dose-related manner typically within 5 min after s.c. injection in male albino rats. Threshold for increased drinking was 1.25 mg/kg, and 2.5 mg/kg elicited half of the maximal drinking response that followed 20 mg/kg. Histamine was not differentially potent for drinking in the day or night phase of the diurnal cycle. Bilateral subdiaphragmatic vagotomy, with the hepatic branch left intact, severely attenuated drinking in response to systemic histamine. Vagotomized rats drank later and less than did normal rats afters doses of histamine between 1.25 and 40 mg/kg. This attenuation was attributed to the destruction of vagal afferent fibers because histamine-elicited drinking was not affected by blockade of vagal efferents with the peripheral anticholinergic atropine methyl nitrate. Drugs antagonistic to peripheral H2 histamine receptors specifically inhibited drinking in response to histamine; i.p. cimetidine or metiamide delayed and decreased drinking after s.c. histamine and temporarily decreased drinking after hypovolemia produced by s.c. polyethylene glycol, but these H2 antagonists failed to inhibit drinking after water deprivation, cellular dehydration, or isoproterenol. Cimetidine or metiamide inhibited drinking in temporal association with a meal of liquid or solid food without slowing the rate of eating and without decreasing food intake. These results constitute the 1st evidence for a peripheral histaminergic determinant of food-related drinking in the rat.