Abstract
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 i.p. hypertonic saline. When access to water was delayed for 1 h after cellular dehydration, Vgx-C rats initiated drinking quickly with normal latency, but a gastric water preload was a more effective stimulus for drinking suppression in Vgx-C than in normal rats; gastric emptying of a water or phenol red solution preload was more rapid in Vgx-C than in normal rats; and 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. 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 safety for ingested water cannot account for the abnormal latency to initiate drinking after cellular dehydration in Vgx-C rats.