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.