A control model of the physiological basis of thirst
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Summary The purpose of these studies was to assess the appropriateness of control groups in previous thirst conditioning studies and to demonstrate that conditioned drinking can be viewed as a classically conditioned appetitive response. In Experiment I (N = 48) thirst was conditioned by the procedure employed by Solomon and Swanson [see Mowrer (11)]. With the use of a “novel cage” group, suppression rather than enhancement of intake was obtained. These and other investigators' results were interpreted in the light of the appropriateness of control groups. In Experiment II (N = 30) rats demonstrated increased water intake at zero hours water deprivation in the presence of an external stimulus previously paired with an increasing motive state. Intakes monitored at half-hour intervals revealed that “low-to-high” drive associated stimuli did not affect overall intake but did induce differentiation in drinking patterns causing first enhancement and then reduction in intake amounts. The results were agreement with Seligman et al. (14) who suggested that elicitation of the prepared mechanism evokes drinking, but water regulation controls do not allow prolonged hyperdipsia.
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Cerebroventricular infusion of P-113, the blocking agent of angiotensin II, into rats for 75 minutes prior to their being allowed to drink, significantly attenuated their water intake when they had been deprived of water for 30 hours. However, a similar infusion had no effect on the food intake in rats fasted for 30 hours. The results indicate a physiological role for angiotensin II in the drinking response of rats deprived of water.
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To determine the effect of prolonged angiotensin II (A-II) infusion on thirst, daily water intake by drinking was measured in dogs during a 4-day control period, a 4-day period of vehicle infusion without A-II, a 10-day period of A-II infusion, and a 4-day recovery period of vehicle infusion without A-II. During the control period and the periods of vehicle infusion in the absence of A-II, daily water intake by drinking in four dogs averaged 118 +/- 20 ml/day (mean +/- SE). During the 10-day period of A-II infusion at the rate of 13.0 ng/kg per min drinking increased to 269 +/- 49 ml/day (paired t; P less than 0.05). Angiotensin II infusion at the rate of 26.0 ng/kg per min produced a sustained increase in water intake in two dogs during an 8-day period of infusion. These results demonstrate that in dogs, prolonged infusion of angiotensin II stimulates the thirst mechanism and that the effect lasts for more than a few days.
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In all organisms water homeostasis is essential for life and is achieved by a balance between water intake and output. Although water output is regulated closely by renal mechanisms and circulating hormones such as the antidiuretic hormone, arginine vasopressin (AVP), it is only through water intake, controlled by thirst, that water deficits can be replenished. Renal water conservation can only minimize further losses. Should thirst and water intake be diminished, or access to water denied, dehydration and eventually death result.
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