Abstract
Our understanding of the physiology of thirst has been enriched by three major advances of the past decade. First, the lateral preoptic area (LPO) has been identified as the osmosensitive zone for the thirst of cellular dehydration. As the result of the remarkably consistent work of Peck and Novin (1971) in the rabbit and of Blass and Epstein (1971) in the rat we know that the LPO must be intact for cell dehydration to induce drinking, and we know that local dehydration of the LPO arouses thirst in animals that are otherwise in water balance. Second, the work of Fitzsimons (1961) and Stricker (1966) has established extracellular volume loss or hypovolaemia as a stimulus of thirst that is coequal with cell dehydration in potency and reliability. As a consequence we are entitled to work within the context of the double depletion hypothesis of thirst (Epstein, Kissileff, and Stellar, 1973) which asserts that thirst is the joint outcome of depletions of both major compartments for water in animals like ourselves. Our problem is now clarified. We must work to understand how each depletion arouses drinking behaviour and to conceive how they interact in the brain to produce the complex phenomenon of thirst.
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Epstein, A.N., Hsiao, S. (1975). Angiotensin as Dipsogen. In: Peters, G., Fitzsimons, J.T., Peters-Haefeli, L. (eds) Control Mechanisms of Drinking. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-61907-6_18
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DOI: https://doi.org/10.1007/978-3-642-61907-6_18
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