The effects of heat acclimation on water intake and urine output responses to thermal
dehydration and other thirst stimuli were studied in male Sprague-Dawley rats. Rats were heat acclimated by continuous exposure to a 34°C environment for at least 6 weeks. Thermal
dehydration-induced thirst was brought about by exposing the heat-acclimated rats and control rats housed at 24°C to a 37.5°C environment for 4 h without access to food or water. Heat acclimation reduced evaporative and urinary water losses and the increases in plasma
sodium and osmolality during thermal
dehydration, which led to a reduction in thermal
dehydration-induced thirst. Heat acclimation reduced the rate of
rehydration following thermal
dehydration but did not alter the final
rehydration level, indicating that heat acclimation does not alter the primary control of thermal
dehydration-induced thirst. Heat acclimation did not alter water intake or urine output following administration of hypertonic saline, which selectively stimulates intracellular thirst, but led to greater water intake following administration of
angiotensin II, which plays an important role in extracellular/volemic thirst, and following water deprivation, which activates both thirst pathways. Cardiovascular responses to
angiotensin II were not altered by heat acclimation. Heat acclimation thus reduces water loss during heat exposure in rats, but does not have major effects on thermal
dehydration-induced or extracellular thirst but does appear to alter volemic thirst.