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1. Intracranial or subcutaneous doses of atropine or atropine methyl nitrate that were fully effective at preventing drinking in response to intracranial carbachol did not block angiotensin-induced drinking. 2. The nicotinic antagonist dihydro-beta-erythroidine given intracranially affected neither angiotensin- nor carbachol-induced drinking. 3. The dopaminergic antagonists haloperidol and spiroperidol injected intracranially blocked angiotensin-induced drinking but did not affect carbachol-induced drinking. 4. Angiotensin- and carbachol-induced drinking were unaffected by alpha- or beta-adrenergic antagonists except at toxic doses. 5. Destruction of catecholaminergic neurones with 6-hydroxydopamine markedly reduced angiotensin-induced drinking, but had relatively little effect on carbachol-induced drinking. 6. Intracranial haloperidol reduced the amount of water drunk in response to overnight deprivation of water, but did not affect feeding in response to overnight starvation or to intracranial noradrenaline. 7. Drinking following overnight water deprivation was unaffected by intracranial alpha- or beta-adrenergic antagonists. 8. Preventing dopaminergic transmission with intracranial haloperidol decreased the water to food ratio of the rat's intake after overnight starvation, whereas increasing the dopamine levels with the combination of FLA-63 and L-DOPA increased the ratio. 9. Intraventricular dopamine in large amounts caused the water-replete rat to drink. 10. It is concluded that among the many functions of dopaminergic systems in the brain is a role in the control of water intake, and that these systems participate in an important way in drinking in response to angiotensin.
1. Intravenous infusion of the individual components of the renin-angiotensin system caused drinking in dogs in water balance. 2. Angiotensin II was the most potent and rapidly acting peptide inducing drinking. The minimum effective rate of infusion was between 8.3 and 16.6 X 10(-12) mole kg-1 min-1 which yield blood levels of angiotensin II that fell well within physiological limits for the dog and were mildly pressor. Angiotensin I and synthetic renin substrate caused less drinking than angiotensin II, and angiotensin III was the least effective dipsogen. 3. Renin caused significant drinking when infused I.V. at a rate of 0.5 u. min-1 for 15 min. Drinking was slower in onset and continued for longer than after other components of the renin-angiotensin system. 4. Within the dose range 1875-15,000 X 10(-12) mole of angiotensin II the amount of water drunk depended more on the rate of infusion than on the duration of the infusion. 5. During an I.V. infusion of angiotensin II lasting 2 hr, the rate of drinking was greatest during the first 15 min. After this declined progressively. 6. A delay of 1 hr after the start of an intravenous infusion of angiotensin II before access to water was allowed, did not significantly reduce the amount of water drunk. Nor did infusion of isotonic saline for 105 min reduce drinking in response to a subsequent infusion of angiotensin II. However, a preload of dilute milk approximately equal in volume to the amount of water normally drunk in response to I.V. angiotensin II significantly reduced drinking. Therefore the dog stopped drinking during long-term infusions of angiotensin II owing to the action of satiety mechanisms and not to tachyphylaxis or fatigue. 7. Intracarotid infusion of angiotensin II, angiotensin I, synthetic renin substrate and angiotensin III, at 40 X 10(-12) mole min-1 also caused drinking. Intakes of water were similar to the intakes after I.V. infusion at six times the arterial rate, except that angiotensin I was relatively less effective by intracarotid infusion than by I.V. infusion. 8. Renin, infused at 0.5 u. min-1 for 15 min, was much less effective by intracarotid infusion than by intravenous. 9. These results are compatible with a role for circulating angiotensin II in the thirst of hypovolaemia or moderate extracellular dehydration.
Drinking and its associated behaviors were studied in rats deprived of fluid for 8,24, or 48 hr. The behavior of rats drinking water could be divided into three successive stages: (a) an initial intense burst of drinking that could not be easily disrupted; (b) intermittent drinking, often distinguished by the brief appearance of conflict behavior directed at the drinking spout; and (c) termination of drinking. Drinking stopped well before the fluid loss, reflected in a sizable extracellular deficit, was restored. Intake of water was terminated when serum hyponatremia and hypoosmolality (and presumably cellular overhydration) developed in temporal continguity with drinking. These and other considerations suggest that the cellular fluid phase exerts significant inhibitory as well as excitatory control over drinking.
1. Drinking by dogs has been studied during and after running on a treadmill, and compared with the drinking produced by NaCl given by stomach tube or intravenously. 2. When water was offered with a delay of more than 5 min after the end of a run producing loss of 30-90 g water by panting, the drinking was similar to that produced by NaCl, assuming that loss of 100 g water produces the same increase in plasma sodium as 15 m-mole NaCl. It is thus possible to explain drinking with a delay after the run as due to loss of water. 3. When water was offered immediately after a run or during pauses in the running there was drinking which cannot be explained as due to loss of water. Although the immediate stimulus to drinking is small, it may cause repeated small drinks by which the evaporative loss of water during running is matched by water intake. 4. Water (10-20 ml./kg body wt.) given by stomach tube before the run reduced or abolished drinking during running. Doses of water sufficient to stop drinking did not cause an increase in urine volume. 5. From these results a figure is produced placing in order mechanisms which may contribute to the control of water balance.
1. Exposure to radiant heat caused dogs to pant and lose water by evaporation at rates of 40-70 g/hr. 2. When water was offered at intervals during the heating, the dogs drank at about half of the opportunities. The individual drinks were small but, by their repetition, loss of water by evaporation during heating was approximately matched by drinking. 3. Water given by stomach tube reduced drinking during a subsequent period of heating. 4. When water was offered more than 15 min after the end of a period of heating, after panting had ceased, drinking occurred only if the water loss exceeded 50-70 g, about 0-6% of the body water. This is regarded as drinking due to loss of water, beyond a threshold of dehydration necessary to stimulate drinking with the dog at rest. When water was offered during heating, drinking occurred with dehydration less than this threshold. 5. The drinking produced by heating was similar to that produced by running (O'Connor, 1975). When the animal ran under heat, panting was more severe and the water loss greater (85-150 g/hr); it was approximately matched by more drinking.
In order to determine the cause of the disrupted feeding pattern in bulbectomized and recovered LH lesioned rats and to study the role of prandial drinking in producing this feeding pattern, feeding and drinking patterns were simultaneously recorded in these lesioned preparations. It was found that in normal rats drinking occurred mainly before and after the meals. In bulbectomized rats, drinking occurred also before and after the meal, but the main part of the meal associated takes place during the numerous short pauses within the meal. In LH recovered rats the meal associated drinking occurred in a very rapid alternation between eating and drinking during feeding bouts (prandial drinking) and not during the meal pauses. It is suggested that the nibbling pattern seen in LH recovered rats as well as in bulbectomized rats is not due to the prandial drinking but results from the loss of an olfactory input to the LH area.
Four rhesus monkeys were examined by ESB for drinking sites in structures that had been previously demonstrated to support drinking behavior. Three yielded a significantly greater proportion of drinking sites than expected from the earlier study, and one yielded significantly less. As the exploration proceeded, the proportion of sites yielding drinking greatly increased in the drinkers and decreased in the nondrinker, and the ratio of stimulus-bound to nonstimulus-bound drinking sites increased in the drinkers but decreased in the nondrinker. Orienting responses decreased in both drinker and nondrinker as exploration proceeded. Two sites that had reliably supported drinking in the restraint chair failed to do so when telestimulated in a free environment, but instead yielded turning, walking, and climbing behavior. The results suggest that ESB-elicited drinking is determined by stimulation of several overlapping neural systems. These probably include ascending dopaminergic and cholinergic systems which are relatively thirst specific, and a nonspecific, cholinergic component of the reticular activating system which triggers the animal to execute a prepotent response which is specific to a given animal with a given history of stimulation under particular enviromental constraints. The learning of stimulus bound drinking is proposed to have its neural locus within the system which mediates the prepotent response, rather than in a thirst system or general activation system.
The effects on feeding and drinking of various doses of droperidol, haloperidol and spiroperidol were studied in a number of paradigms. All three buryrophenones produced generally similar effects. After food deprivation, feeding was slightly increased at low doses but was decreased at the higher doses; the concomitant postprandial drinking was attenuated at all doses. Desalivate rats showed a marked attenuation of feeding (and prandial drinking) at low doses, but when wet mash was given instead of pellets and water a normal dose-response relationship was obtained. After water deprivation drinking was attenuated at all doses, and when food was also available during the drinking test the food intake was decreased in proportion to the drinking. Drinking was blocked more when food was present than in its absence. Insulin and 2-deoxyglucose induced feeding in sated rats was attenuated but not abolished by haloperidol. The findings are discussed relative to the role of activation and brain catecholamines in feeding and drinking.