Related Experiment Videos
Intraperitoneal administration of recombinant human interleukin-1 beta inhibits osmotic thirst in the rat
1Department of Physiology, University of Occupational and Environmental Health, Kitakyushu, Japan.
Decrease in water intake after intraperitoneal injection of interleukin-1 beta (IL-1 beta) was studied in the rat. Administration of IL-1 beta at a dose of 20 micrograms/kg attenuated osmotic thirst induced by intraperitoneal injection of hypertonic saline, but did not affect hypovolemic thirst induced by subcutaneous injection of either polyethylene glycol or angiotensin II. Interleukin-1 beta also decreased spontaneous intake of water but not that of 1.8% saline. The results suggest that the decrease in water intake by IL-1 beta is caused, at least in part, by suppression of osmotic thirst but not by general suppression of behavior. The effects of IL-1 beta were not secondary responses accompanied by feeding behavior, since food supply was removed during the experiments. Pretreatment with indomethacin blocked the decrease in water intake by IL-1 beta, suggesting the involvement of production of prostaglandins.
Decrease in water intake after intraperitoneal injection of interleukin-1 beta (IL-1 beta) was studied in the rat. Administration of IL-1 beta at a dose of 20 micrograms/kg attenuated osmotic thirst induced by intraperitoneal injection of hypertonic saline, but did not affect hypovolemic thirst induced by subcutaneous injection of either polyethylene glycol or angiotensin II. Interleukin-1 beta also decreased spontaneous intake of water but not that of 1.8% saline. The results suggest that the decrease in water intake by IL-1 beta is caused, at least in part, by suppression of osmotic thirst but not by general suppression of behavior. The effects of IL-1 beta were not secondary responses accompanied by feeding behavior, since food supply was removed during the experiments. Pretreatment with indomethacin blocked the decrease in water intake by IL-1 beta, suggesting the involvement of production of prostaglandins.