285 290 295 300 305 Plasma osmolality (mOsm kg -1)

Figure 7 The relationship of plasma vasopressin (o) and thirst (x) to plasma osmolality in a volunteer during infusion of 5% saline. (Redrawn with permission from Robertson GL (1984) Abnormalities of thirst regulation (Nephrology forum). Kidney International 25: 460-469.)

respective osmoreceptors to the thirst centers and the arginine vasopressin-releasing centers. Within the normal range for plasma osmolality, the inhibitory and excitatory activities in the thirst centers effectively cancel out one another and there is neither a sensation of thirst or satiety. However, at this level of activity there is release of a basal level of arginine vasopressin that is sufficient to maintain a state of half-maximum antidiuresis. A rise in plasma osmolality above the normal level stimulates greater excitatory output causing an increase in the feeling of thirst and higher levels of circulating arginine vasopressin. Raised levels of arginine vasopressin increase the concentrating ability of the kidneys. A decrease in plasma osmolality below the normal range increases the inhibitory output producing a feeling of satiety, and arginine vasopressin release is suppressed allowing urinary dilution (Figure 3).

Cells and fibers within the brain have been shown to contain several hormones, including angiotensin and vasopressin, within the same cell. Although neurons associated with the thirst centers can be activated in vitro by vasopressin, it is not clear whether peripheral- or neural-generated arginine vasopressin levels influence the perception of thirst.

Volemic Regulation of Thirst

The receptors that initiate hypovolemic thirst are generally thought to be the cardiovascular barore-ceptors, which respond to underfilling of the circulation by reducing their inhibitory nerve impulse activity to the thirst centers. However, in areas of the brain associated with the thirst centers there are neurons that are separately responsive to volemic, pressure, and osmotic changes. This suggests that at least part of the response to changes in blood volume originates in the brain. It is thought that changes in blood pressure and osmolality are monitored mainly within the brain, whereas variations in blood volume are principally sensed by the peripheral baroreceptors, with a degree of overlap between the different receptors. The mechanisms that respond to changes in intravascular volume and pressure appear to be not as sensitive as those responsive to osmotic changes; for example, a decrease of approximately 10% of the plasma volume is required to initiate hypovolemic thirst. Because fairly large variations in blood volume and pressure occur during normal daily activity, such as postural changes and physical activity, this apparent lack of sensitivity presumably prevents overactivity of the volemic control mechanisms. As with osmotic thirst, the control of volemic thirst is thought to be a balance between continuous inhibitory and excitatory neural activity, although in this system the basal level appears to be essentially inhibitory. Another difference in the basic control mechanism between the two systems is due to the requirement for both solute, mainly sodium, and water to restore the extracellular volume. Therefore, extracellular dehydration causes an initial thirst and a delayed increase in sodium appetite.

Reduction in the intravascular volume sufficient to lower cardiac output and arterial blood pressure decreases afferent activity from the low- and high-pressure cardiovascular baroreceptors to the thirst centers and increases sympathetic activity to the kidneys. Because afferent input from the barorecep-tors to the thirst centers is inhibitory, a decrease in activity produces a reflex increase in the perception of thirst and also appears to directly stimulate argi-nine vasopressin release. The increase in sympathetic activity to the kidneys directly promotes greater renal renin release. In addition, reduction in blood pressure lowers the renal perfusion pressure, which stimulates renin release both as a direct pressure effect and by decreasing the delivery of sodium to the kidneys.

Increased activation of the renin-angiotensin-aldosterone system also helps regulate hypovolemic thirst. While circulating levels of both vasopressin and aldosterone affect water and sodium reabsorption in the kidneys and thereby control water and solute loss, angiotensin acts directly on the thirst and sodium appetite centers to stimulate their respective responses. Neurons that are stimulated by angioten-sin are found in areas of the brain that lack a blood-brain barrier; therefore, circulating angiotensin has direct access to both centres. In addition, the release of neurally generated angiotensin is promoted by suitable neuron activity responding to sensory stimuli (Figure 4).

There are a variety of neural and hormonal responses that interact to modulate and control both thirst and urine excretion. A number of other hormones, including oxytocin, atrial natriuretic pep-tide, tachykinins, neuropeptide Y, thyroid hormones, corticotrophin-releasing factor, and steroid hormones, have also been shown experimentally to affect the drinking response. Under normal conditions of water and solute loss, both osmotic and volemic dehydration occur; therefore, stimuli from receptors for both systems are usually involved in the sensation of thirst. Increases in extracellular osmolality appear to be more effective than hypovo-lemia in promoting the thirst and hence drinking response. More than 70% of the stimulus to drink appears to be generated by increased osmolality.

Sensory Regulation of Thirst

The sensations of a dry mouth or desire for a specific taste or effect also generate the desire to drink when there may be no physiological requirement to drink. A dry mouth promotes changes in neural activity in the parahippocampus, amygdala, thalamus, cingulate, insula, allocortex, and transitional cortex of the brain. This finding has strengthened the hypothesis that the perception of thirst is a primitive vegetative function that appeared long before vertebrates evolved.

Drinking water activates areas of the anterior insular and frontal opercular cortex that are also involved in the perception of taste. Areas of the orbitofrontal cortex are also activated by the ingestion of water or sweet or salty tastes, but activation is greatest when subjects are thirsty and it diminishes when subjects have drunk water to satiety. This has been interpreted as functionally separate areas of the brain, one of which responds to taste stimuli that are not diminished following drinking to satiety, whereas the other is highly active during drinking when water is physiologically required but reduces as the need for water is met.

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