Abdominal vagotomy inhibits osmotically induced drinking in the rat.

After complete bilateral transection of the abdominal vagus (Vgx-C), with the hepatic branch left intact, rats drank later and less than normal after cellular dehydration induced by intraperitoneal hypertonic saline. When access to water was delayed for 1 hr after cellular dehydration, Vgx-C rats initiated drinking quickly with normal latency, but (a) a gastric water preload was a more effective stimulus for drinking suppression in Vgx-C than in normal rats; (b) gastric emptying of a water or phenol red solution preload was more rapid in Vgx-C than in normal rats; and (c) when gastric emptying dysfunction in Vgx-C rats was removed by having rats sham drink, Vgx-C and normal rats sham drank equivalent amounts of water. Thus, disordered preabsorptive satiety caused by abnormally rapid gastric emptying of water is a factor in the decreased drinking of Vgx-C rats after cellular dehydration. Disordered satiety for ingested water cannot, however, account for the abnormal latency to initiate drinking after cellular dehydration in Vgx-C rats.