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.
The effect of electrical brain stimulation (ESB; 50 Hz, 50-150 microA sine wave, 5 s on/5 s off) on osmotic thirst was examined in 10 conscious dogs chronically implanted with electrodes aimed at the anteromedial part of the basal forebrain. Suppression of osmotic thirst (SOT) was observed during stimulation through 18 of 41 electrodes located in the olfactory tubercle, the nucleus accumbens, the caudate nucleus, the medial septum, and the lateral preoptic-anterolateral hypothalamic area (PrA/ALH). Mean increment in plasma osmolality necessary to cause drinking rose from 9.0 +/- 1.5 mosmol (X +/- SE; n = 15) under control conditions to 15.8 +/- 2.6 mosmol (n = 18) during ESB in SOT placements. Threshold cellular dehydration eliciting drinking increased from 2.70 +/- 0.50% of intracellular water (ICW;n = 16) to 4.77 +/- 0.68% of ICW (n = 18), respectively. The strongest SOT was found during ESB in the nucleus accumbens, and the PrA/ALH. The same stimulation failed to inhibit feeding, support self-stimulation or produce appreciable changes of dog's gross behavior. The results give evidence for the existence in the basal forebrain of the dog a widely distributed neural system suppressing osmotic thirst. The nucleus accumbens and the PrA/ALH seem to play an important role in this system.
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