AJP - Regulatory, Integrative and Comparative Physiology, Vol 242, Issue 5 423-R428, Copyright © 1982 by American Physiological Society
Physiological mechanisms for thirst in the nonhuman primate
R. J. Wood, E. T. Rolls and B. J. Rolls
The relationship between body fluid deficits and drinking has been
investigated in a nonhuman primate. Intravenous sodium chloride infusions
(0.93-3.25 M) given to rhesus monkeys caused drinking correlated with
increases in plasma osmolality and sodium concentrations. Sucrose infusions
(0.3 M in 0.15 M NaCl) also caused drinking while equiosmolal urea
infusions did not. It was found that the drinking threshold corresponded to
a 2.3% increase in plasma osmolality. Water deprivation for 24 h caused
significant cellular dehydration, as indicated by a 5.8% elevation in
plasma osmolality that exceeded the threshold for thirst, and a significant
hypovolemia as indicated by elevated plasma protein and hematocrit values.
Intravenous water preloads decreased plasma osmolality and produced a
dose-related decrease in subsequent drinking. Infusions that restored
plasma osmolality to predeprivation values, reduced intake by 85%.
Intravenous isotonic saline preloads which abolished the hypovolemia did
not have a consistent effect and reduced mean water intakes by only 3.2%.
Thus in the rhesus monkey, cellular dehydration is an effective stimulus
for thirst, and it is the primary determinant of drinking after water
deprivation, used as an example of a natural thirst stimulus. In contrast
to findings in nonprimates, the extracellular deficit contributes very
little to drinking after water deprivation.
