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- W71113098 abstract "Publisher Summary Hypovolemia, or mimicking its effect by reducing the venous return to the heart by obstructing the inferior vena cava, causes increased thirst and, after a delay of some hours, increased sodium appetite. These two behavioral responses, together with the mobilization of fluid from the tissues and gut, reduction in urine flow, and redistribution of cardiac output, enable the body to withstand and correct the hypovolemia. This chapter reviews that the significant positive correlations between drinking and the fall in central venous pressure and in arterial pressure suggest that stretch receptors in the circulation are involved in hypovolemic thirst. Afferent impulses from volume receptors and baroreceptors are inhibitory to thirst. Besides being involved in drinking behavior, stretch receptors in the circulation also influence the secretion of renin through their effect on sympathetic tone to the kidney. The possible involvement of the renin–angiotensin system in hypovolemic thirst is examined in the chapter, since renin itself causes drinking in the absence of changes in stretch receptor stimulation." @default.
- W71113098 created "2016-06-24" @default.
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- W71113098 date "1981-01-01" @default.
- W71113098 modified "2023-09-23" @default.
- W71113098 title "THE ROLE OF ANGIOTENSIN II IN THE CONTROL OF HYPOVOLAEMIC THIRST AND SODIUM APPETITE" @default.
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- W71113098 doi "https://doi.org/10.1016/b978-0-08-026824-8.50078-3" @default.
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