Dehydration-induced drinking in humans.

Abstract

Mechanisms of drinking have been studied extensively in laboratory mammals, but comparatively little information is available on human consumption of fluids. The assumption that osmotic disequilibrium between extra- and intracellular fluid can be rectified within seconds may not be true for plasma and red blood cell (RBC) fluid in humans inasmuch as stress-induced hyperosmotemia to +13 mosmol/kg does not cause a significant change in mean RBC corpuscular volume. Unlike some mammals, humans have a delay in rehydration (involuntary dehydration) after fluid loss. Two factors unique to humans that probably contribute to involuntary dehydration are 1) upright posture and 2) extracellular fluid and electrolyte loss by sweating from exercise and heat exposure. If drinking is influenced by upright postural changes, it may be related to increased plasma renin activity (PRA) but not to increases in plasma osmolality or arginine vasopressin concentration. Under combined stresses of heat, exercise, and prior dehydration, exercise is the greatest inhibiting factor and heat exposure has the least inhibitory effect on voluntary water intake. The rate of drinking during exercise in heat has a high correlation with sweat rate but is essentially unrelated to the well-established dipsogenic factors of plasma volume, osmolality, and PRA. However, it is likely that some or all of these dipsogenic factors act to initiate drinking in humans.