The extracellular fluid becomes hyperosmotic with water deprivation, leading to hyperosmotic intracellular fluid. Osmoreceptors in the brain detect the increase in osmotic pressure of the extracellular fluid. These osmoreceptors are located in the organum vasculosum of the lamina terminalis, a circumventricular organ. The subfornical organ and the organum vasculosum are involved in thirst.

Water deprivation also results in a decrease in blood volume, which is sensed by receptors in the low-pressure side of the vasculature, including the right atrium of the heart. This triggers the release of renin by the kidneys. Renin breaks down angiotensinogen into angiotensin I, which is then hydrolyzed to angiotensin II. Angiotensin II stimulates drinking by acting on angiotensin II receptors in the subfornical organ, another circumventricular organ. Angiotensin II also causes vasoconstriction and the release of aldosterone and antidiuretic hormone (ADH).

Excessive water intake is easily eliminated by inhibiting the release of ADH from neurons in the supraoptic nucleus at their terminals in the posterior pituitary gland. Signals that inhibit ADH release include increased blood volume and decreased osmolality of extracellular fluid. The preoptic region and lateral hypothalamus, along with structures outside the hypothalamus, also regulate water intake.

The central nucleus of the amygdala, the bed nucleus of the stria terminalis, and various areas of the cerebral cortex, in addition to the hypothalamus, play a role in autonomic control. Information from the viscera reaches these higher autonomic centers through an ascending system involving the nucleus of the solitary tract, the parabrachial nucleus, the periaqueductal gray matter, and the hypothalamus. Descending pathways originating from structures such as the paraventricular nucleus of the hypothalamus, noradrenergic cell group A5, the rostral ventrolateral medulla, and the raphe nuclei and adjacent structures of the ventromedial medulla help control autonomic activity.

Environmental stress can cause immunosuppression, reducing the number of helper T cells and the activity of natural killer cells. Corticotropin-releasing factor released from the hypothalamus can induce immunosuppression by stimulating the release of adrenocorticotropic hormone (ACTH) from the pituitary gland, which in turn triggers the secretion of adrenal corticosteroids. Direct neural actions on lymphoid tissue can also contribute to immunosuppression. Additionally, the immune system can influence neural activity.
Fig. 11.5
With water deprivation, the extracellular fluid becomes hyperosmotic, which in turn causes the intracellular fluid to become hyperosmotic. The brain contains neurons that serve as osmoreceptors for detection of increases in the osmotic pressure of extracellular fluid (see also ). The osmoreceptors appear to be located in the organum
Angiotensin II receptors Angiotensin II receptors Osmotic receptors Blood vessels Drinking circuit, including vasopressin-releasing neurons in the posterior pituitary B •Fig. 11.5 A, Structuresthoughttoplayaroleintheregulationofwaterintakeinrats.LHA,lateralhypothalamicarea.B, Neuralcircuitsthatsignalchangesinbloodosmolalityandvolume.(A, RedrawnfromShepherdGM.Neurobiology. NewYork:OxfordUniversityPress;1983.) vasculosum of the lamina terminalis, which is a circumventricular organ. Circumventricular organs surround the cerebral ventricles and lack a blood-brain barrier. The subfornical organ and the organum vasculosum are involved in thirst.
Water deprivation also causes a decrease in blood volume, which is sensed by receptors in the low-pressure side of the vasculature, including the right atrium of the heart (see also ). In addition, decreased blood volume triggers the release of renin by the kidneys. Renin breaks down angiotensinogen into angiotensin I, which is then hydrolyzed to angiotensin II (see ). This peptide stimulates drinking by an action on angiotensin II receptors in another of the circumventricular organs, the subfornical organ. Angiotensin II also causes vasoconstriction and release of aldosterone and antidiuretic hormone (ADH).
Insufficient water intake is usually a greater problem than excessive water intake. However, when more water is taken in than required, it is easily eliminated by inhibition of the release of ADH from neurons in the supraoptic nucleus at their terminals in the posterior pituitary gland (see ). As mentioned previously, signals that inhibit release of ADH include increased blood volume and decreased osmolality of extracellular fluid. Other areas of the hypothalamus, particularly the preoptic region and lateral hypothalamus, help regulate water intake, as do several structures outside the hypothalamus.
Several regions of the forebrain other than the hypothalamus also play a role in autonomic control. These regions include the central nucleus of the amygdala and the bed nucleus of the stria terminalis, as well as a number of areas of the cerebral cortex. Information reaches these higher autonomic centers from viscera through an ascending system that involves the nucleus of the solitary tract, the parabrachial nucleus, the periaqueductal gray matter, and the hypothalamus. Descending pathways that help control autonomic activity originate in such structures as the paraventricular nucleus of the hypothalamus, noradrenergic cell group A5, the rostral ventrolateral medulla, and the raphe nuclei and adjacent structures of the ventromedial medulla.
Neural Influences on the Immune System
Environmentalstresscancauseimmunosuppression,inwhich the number of helper T cells and the activity of natural killer cells are reduced. Immunosuppression can even be the result of classical conditioning. One mechanism for such an effect involves the release of corticotropin-releasing factor from the hypothalamus. Corticotropin-releasing factor causes the release of adrenocorticotropic hormone (ACTH) from the pituitary gland; release of ACTH stimulates the secretion of adrenal corticosteroids, which cause immunosuppression (see ). Other mechanisms include direct neural actions on lymphoid tissue. The immune system may also influence neural activity.
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