Abstract
Stimuli such as hypovolemia or hypotension which increase the secretion of renin from the kidneys increase thirst in man and other vertebrates1. However, intravenous infusions of renin or angiotensin II (Ang II) at doses which produce circulating concentrations similar to those observed in hypovolemia and hypotension cause relatively little drinking2,3,4. This could be interpreted to mean that the role of Ang II in the control of drinking to these stimuli is minor. The conditions are not comparable, however. Intravenous infusions of Ang II cause large increases in arterial pressure in the water-replete animal whereas under physiological conditions these same concentrations of Ang II would occur when blood pressure was at or below normal.
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© 1986 Springer Science+Business Media New York
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Robinson, M.M., Evered, M.D. (1986). Angiotensin II and Arterial Pressure in the Control of Thirst. 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_26
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DOI: https://doi.org/10.1007/978-1-4757-0366-5_26
Publisher Name: Springer, Boston, MA
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