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Published online by Cambridge University Press: 09 December 2021
Acute depletion of ECF volume without change in osmolality is sufficient to induce drinking in many species. However, the threshold for drinking appears to be quite large, of the order 10–20% loss of plasma volume. This change may occur without significant drop in arterial pressure, due to effective physiological counter-regulation, including secretion of renin from the kidneys and subsequent generation of ANG II. Under many conditions of actual or simulated hypovolemia, ANG II appears to be involved in the drinking response and probably by action on AT1a receptors in the SFO. However, interference with ANG II production and/or action does not uniformly disrupt all forms of hypovolemia-related drinking, and it appears that afferents from cardiopulmonary pressure receptors may also be involved. There may be strain differences in the relative contribution of these two mechanisms, or others, to extracellular dehydration drinking. Restoration of ECF volume requires ingestion of NaCl as well as water, and mechanisms for this are discussed briefly.
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