Abstract and Keywords
Maintaining water balance is critical for survival, but our bodies are constantly losing more water than we produce. Consuming water, therefore, is needed to restore what is lost by sweating, bleeding, vomiting, urinating, even breathing. Because the fluid in the body is divided into intracellular and extracellular compartments, and because depletion can happen in one compartment without affecting the other, separate detection mechanisms for losses in each are required. Moreover, the relatively high concentration of sodium in the extracellular space means that sodium loss accompanies extracellular dehydration. Accordingly, the behavioral response to loss of fluid from the extracellular space needs to include sodium intake. Activity of osmoreceptors (in the case of intracellular loss), or baroreceptors and the renin-angiotensin system (in the case of extracellular loss), underlies the responses to perturbations of fluid balance, and promotes the appropriate behaviors needed to restore balance to the system. The peptide angiotensin II (AngII) is a key component of these responses. Studies of AngII in drinking have been critical in our understanding of how a peripherally derived peptide can act in the brain without transport across the blood–brain barrier, and AngII-induced drinking has served as an important model for the study of intracellular signaling pathways that affect behavior. Although much has been discovered about these systems and how they respond to fluid deficits, the precise means by which the systems generate a behavioral response and the mechanism that mediates satiety remains poorly understood. Nevertheless, ongoing experiments on these open questions have already started to provide a new perspective on the negative reinforcement that is provided by drinking under conditions of thirst.
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