Areas of the hypothalamus and forebrain, that are collectively termed the thirst control centers, appear to be central to the regulation of both thirst and diuresis. Receptors in the thirst control centers respond directly to changes in osmolality, volume, and blood pressure, while others are stimulated by the fluid-balance hormones that also regulate renal excretion. These regions of the brain also receive afferent input from systemic receptors monitoring osmolality, circulating sodium concentration, and alterations in blood volume and pressure. Changes in the balance of neural activity in the thirst control centers regulated by the different monitoring inputs determine the relative sensations of thirst and satiety, and influence the degree of diuresis. Input from the higher centers of the brain, however, can override the basic biological need for water to some extent and cause inappropriate drinking responses. Cases of water intoxication (hyponatremia) during endurance sports events lasting more than about 6-8 h have been reported in which the major cause of the illness is due to overhydration as a result of overdrinking.
A rise of between 2 and 3% in circulating osmolality (i.e., about 6-8mosmkg~1 H2O) is sufficient to evoke a profound sensation of thirst coupled with an increase in the circulating concentration of antidiuretic hormone, also known as vasopressin. The mechanisms that respond to changes in intra-vascular volume and pressure appear to be less sensitive than those that monitor plasma osmolality, with hypovolemic thirst being evident only following a 10% decrease in blood volume. As fairly large variations in blood volume and pressure occur during normal daily activity, primarily in response to postural changes, this lack of sensitivity presumably prevents overactivity of the volume-control mechanisms. Prolonged exercise, especially in the heat, is associated with a decrease in plasma volume and a tendency for an increase in osmolality, but fluid intake during and immediately following exercise is often less than that required to restore normal hydration status. This appears to be due to a premature termination of the drinking response rather than to a lack of initiation of that response. Also, the composition of the beverage consumed has an effect on the volume of fluid ingested, with water prematurely abolishing the osmotic drive to drink, while sodium-containing drinks help maintain the osmotic drive to drink and increase voluntary intake.
When a water deficit is present and free access to fluid is allowed, the drinking response in man usually consists of a period of rapid ingestion, during which more than 50% of the total intake is consumed, followed by intermittent consumption of relatively small volumes of drink over a longer period. The initial alleviation of thirst occurs before significant amounts of the beverage have been absorbed and entered the body water. Therefore, although decreasing osmolality and increasing extracellular volume promote a reduction in the perception of thirst, other preabsorptive factors also affect the volume of fluid ingested. Receptors in the mouth, oesophagus, and stomach are thought to meter the volume of fluid ingested, while distension of the stomach tends to reduce the perception of thirst. These preabsorptive signals appear to be behavioural, learned responses and may be subject to disruption in situations which are novel to the individual. This may partly explain the inappropriate voluntary fluid intake in individuals exposed to an acute increase in environmental temperature or to exercise-induced dehydration.
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