Central dipsogenic effect of vasopressin.
The purpose of the present study was to investigate the possible role of vasopressin (ADH) in the control of thirst. With this aim spontaneous water intake (WI) was examined in conscious dogs after 1) electric stimulation in the basal forebrain causing release of ADH, 2) injection of 0.03, 0.05, 0.10, 0.15, 0.30, and 3.00 mU of ADH into the third cerebral ventricle (3rd V), 3) injection of 0.3, 3.0, and 30 mU of ADH into the lateral cerebral ventricle (LV) and injection of 5.0 and 10.0 mU of ADH into the carotid artery (CA). Stimulation through 10 of 16 electrodes located in various structures of the limbic system caused a significant increase in blood ADH, decrease of urine output, increase in renal free-water reabsorption, nonstimulus-bound drinking, positive water balance, and decrease in plasma osmolality (Posmol). Injection of ADH to the 3rd V caused a significant increase in WI. The maximum WI was observed after injection of 0.10-0.15 mU of ADH. Elevation of WI caused a significant decrease in Posmol 1 h after injection of ADH to the 3rd V. Insignificant increases or no changes in WI were observed when ADH was injected into the LV and CA, respectively. The results suggest that ADH may exert central dipsogenic effects.
D000818:Animals; D002552:Cerebral Ventricles / Q000502:physiology*; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D004327:Drinking Behavior / Q000502:physiology*; D004558:Electric Stimulation; D004567:Electrodes, Implanted; D007276:Injections, Intraventricular; D008032:Limbic System / Q000502:physiology; D008297:Male; D013894:Thirst / Q000502:physiology*; D014667:Vasopressins / Q000008:administration & dosage / Q000494:pharmacology*
D014667:Vasopressins