Abstract
There is considerable evidence that intravascular volume is monitored by the low pressure stretch receptors found in the atria and great veins near the heart.1 Thus it was gratifying, but not altogether surprising, to confirm that stimulation of these receptors attenuated drinking to extracellular fluid deficits but was without effect on drinking to intracellular fluid deficits.2 However, maintenance of extracellular fluid volume depends upon the ability to regulate not just water but also salt balance. A study was therefore made of the effect on salt appetite of stimulating the right atrial receptors. Since there is evidence that the renin-angiotensin system is involved in regulating salt intake3, two very different models of salt appetite were investigated. The first, namely sodium depletion by removal of isotonic fluid, results in activation of the renin-angiotensin system4,5. In the second experiment, salt appetite was induced by injection of deoxycorticosterone acetate (DOCA). Under these circumstances the renin-angiotensin system is known to be suppressed6.
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References
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© 1986 Springer Science+Business Media New York
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Kaufman, S. (1986). Contol Mechanisms of Salt Appetite. In: de Caro, G., Epstein, A.N., Massi, M. (eds) The Physiology of Thirst and Sodium Appetite. NATO ASI Series, vol 105. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-0366-5_60
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DOI: https://doi.org/10.1007/978-1-4757-0366-5_60
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4757-0368-9
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