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of isotonic saline, three-fourths would come from the interstitial fluid and one-fourth would come from the plasma fluid.

Gilman (1937) demonstrated that intravenous infusions of hyperosmotic sodium chloride elicited drinking but that equally hyperosmotic solutions of urea stimulated thirst poorly. Since urea could diffuse into cells but sodium would produce shrinkage, an osmotic basis for thirst was established. Other solutes that cause the withdrawal of water from cells, such as sucrose and sorbitol, were equally effective in producing thirst when infused intravenously (Holmes and Gregersen, 1950a,b). These observations reinforced the important role of cellular dehydration in triggering thirst and drinking behavior. The classic work of Verney (1947) demonstrated that water diuresis in dogs could be inhibited by intracarotid infusions of hypertonic sodium chloride and, therefore, that both thirst and antidiuresis were linked to the osmotic withdrawal of water from cells. Verney (1947) deduced that the inhibition of water diuresis resulted from neurohypophyseal secretion of vasopressin, which was later confirmed (Wade et al., 1982). According to Andersson (1978), the most potent stimulators of antidiuretic hormone (ADH) release and thirst are absolute and relative dehydration. Although ADH is released as a function of the body osmolality (Robertson and Athar, 1976; Robertson and Mahr, 1972), it is equally well correlated with plasma sodium (Olsson et al., 1978).

Andersson (1978) suggested that sodium itself is the crucial factor in the osmotic control of water balance and proposed that the centrally located osmoreceptors are responding to specific changes in the cerebrospinal fluid (CSF) sodium concentration subsequent to perturbations in the extracellular fluid osmolality. This was supported by the observation that hypertonic sucrose did not stimulate thirst and ADH when infused into the third ventricle (Olsson, 1969). Intracerebral infusions of hypertonic sucrose can inhibit ADH release by dilution-reduction of the CSF sodium concentration, which argues against a receptor location outside the blood-brain barrier. Andersson (1978) recognized that there is the possibility that both elevated sodium and cellular dehydration trigger a biochemical process involved in the receptor-excitation mechanism. Andersson (1978) further suggested that angiotensin II might be an activator of a cationic transporting enzyme. Angiotensin II (Gutman et al., 1972), L-norepinephrine (Desaiah and Ho, 1977), and prostaglandin PGE1 (Limas and Cohn, 1974) interact with sodium, possibly at the level of Na-K-adenosine triphosphatase (ATPase), in stimulating ADH and thirst.

The ADH of humans and most other mammals is arginine vasopressin, which is produced by the neurohypophysis. Under physiological conditions, ADH release is apparently controlled primarily by plasma osmolality, but the osmoregulatory system appears to display large individual (Robertson, 1977;

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