Histamine-elicited drinking is dependent upon gastric vagal afferents and peripheral angiotensin II in the rat

Abstract

While transection of either the anterior (including hepatic) or posterior (including coeliac) vagal trunk failed to alter drinking in response to subcutaneous histamine (0.312–20 mg/kg), selective gastric vagotomy severely attenuated drinking after systemic histamine (1.25–40 mg/kg) in male Sprague-Dawley rats. The dose-response curve for rats with gastric vagotomy was shifted to the right: Vagotomy increased the threshold dose nearly tenfold and more than doubled the ED 50. Because the effect of vagotomy on histamine-elicited drinking was not mimicked by cholinergic blockade of vagal efferents using atropine methyl nitrate (10 mg/kg), these results demonstrate that gastric vagal afferents are necessary for a normal drinking response to systemic histamine. When gastric vagotomy was combined with intragastric SQ14,225 (to inhibit the conversion of peripheral angiotensin I to angiotensin II) drinking after systemic histamine was abolished. These results suggest that gastric vagal afferents and angiotensin II are necessary for systemic histamine to elicit drinking in the rat.