Parotid glands (PGs) are atrophied markedly by long-term feeding of liquid diets. These atrophied PGs recovered to normal size with a solid diet in few days. To investigate the mechanism of this PG recovery, we compared PG weight and acetylcholine-induced salivary secretion in three groups of Wistar rats: 1) a group fed a solid diet for 17 days (control group), 2) a group fed a liquid diet for 17 days (atrophic group), and 3) a group fed a liquid diet for 14 days followed by the solid diet for 3 days (recovery group). The PG weight and salivary secretion in the atrophic group were decreased to 35 and 58% of the control group, respectively, whereas in the recovery group, they recovered to 84 and 120% of the control group, respectively. We thought that oral sensory stimulation by solid diet recovers salivary gland functions via the autonomic nervous system, and thus we examined the effects of pilocarpine (Pilo), isoprenaline (ISO), and nicotine (Nic) on the recovery of atrophic glands. Subcutaneous administrations of these reagents during the last 3 days of liquid diet feeding recovered PG, and PG weight of Pilo-, ISO-, and Nic-treated group was 78, 121, and 78% of the control group, respectively. These results indicate the involvement of autonomic neurotransmitters in the self-recovery mechanism by oral sensory stimulation.