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Thirst center

The osmoreceptors of the hypothalamus monitor the osmolarity of extracellular fluid. These receptors are stimulated primarily by an increase in plasma osmolarity they then provide excitatory inputs to the thirst center and the ADH-secreting cells in the hypothalamus. The stimulation of the thirst center leads to increased fluid intake. The stimulation of the ADH-secreting cells leads to release of ADH from the neurohypophysis and, ultimately, an increase in reabsorption of water from the kidneys and a decrease in urine output. These effects increase the water content of the body and dilute the plasma back toward normal. Plasma osmolarity is the major stimulus for thirst and ADH secretion two additional stimuli include ... [Pg.339]

A more moderate stimulus for thirst and ADH secretion is a decrease in extracellular fluid, or plasma volume. This stimulus involves low-pressure receptors in the atria of the heart as well as baroreceptors in the large arteries. A decrease in plasma volume leads to a decrease in atrial filling, which is detected by low-pressure receptors, and a decrease in MAP, which the baroreceptors detect. Each of these receptors then provides excitatory inputs to the thirst center and to the ADH-secreting cells. [Pg.339]

Angiotensin II also stimulates the thirst center to increase the urge to ingest fluids, and ADH secretion to promote reabsorption of water from the kidneys. Other factors influencing ADH-secreting cells (but not the thirst center) include pain, fear, and trauma, which increase ADH secretion, and alcohol, which decreases it. [Pg.339]

Angiotensin II has a variety of effects. By constricting blood vessels it raises blood pressure, and by stimulating thirst centers in the brain it increases blood volume. Both angiotensins II and III also act on the adrenal gland to promote the synthesis and release of aldosterone. Most of the effects of angiotension II are mediated by 359-residue seven-helix G-protein linked receptors which activate phospholipase C.p q qr Like other steroid hormones aldosterone acts,via mineralocorticoid receptors, to control transcription of a certain set of proteins. The end effect is to increase the transport of Na+ across the renal tubules and back into the blood. Thus, aldosterone acts to decrease the loss of Na+ from the body. It promotes retention of water and raises... [Pg.1261]

Water intoxication has been reported during treatment with thioridazine and may be due to its pronounced anticholinergic properties and/or direct stimulation of the hypothalamic thirst center (21). [Pg.364]

The thirst center is regulated by many of the same factors that determine AVP release. This center has a higher set point than the osmoreceptors and responds to osmolalities above 290mOsm/kg. Responses involving AVP, thirst, and the kidney are coordinated in a complex scheme to maintain plasma osmolality in healthy individuals within a narrow range (284 to 295mOsm/kg). [Pg.1992]

Psychogenic or Primary Polydipsia. A chronic, excessive intalce of water suppresses AVP secretion and produces hypotonic polyuria. The polyuria and polydipsia are usually not as sustained as in HDI or NDI nocturnal polyuria also is less frequent. Psychogenic factors are most commonly associated with this disorder, but hypothalamic disease affecting the thirst center may be a cause. Drugs also can affect the thirst center and result in primary polydipsia. [Pg.1992]

The thirst center in an attempt to restore volume through increased intake... [Pg.88]

Psychogenic DI—excessive water intake resulting from a psychologic disorder or a lesion in the thirst center... [Pg.213]

Thirst (in humans) is the conscious desire for water. It is the primary means of regulating water intake, and generally, the thirst sensation ensures that water intake meets or exceeds the body s requirement for water. The sensation of thirst is caused by nerve centers in the hypothalamus of the brain which monitor the concentration of sodium (osmolar-ity) in the blood. When the sodium concentration of the blood increases abiove the normal 310 to 340 mg/100 ml (136 to 145 mEq/1), cells in the thirst center shrink. This shrinking causes more nervous impulses to be generated in the thirst center, thereby creating the sensation of thirst. An... [Pg.1020]

The body is equipped with a number of mechanisms for regulating body water within narrow limits. Important among these mechanisms are nerve centers in the hypothalamus of the brain which control the sensation of thirst and water output by the kidneys. Stimulation of the thirst center in the hypothalamus results when water loss amounts to about 1% of the body weight, and creates the conscious desire for water. If water is not drunk, discomfort increases—heart rate increases, body temperature rises, and working and thinking abilities deteriorate. Heat exhaustion is certain if physical work is attempted when water loss Is 10% of the body weight. Stimulation of other nerve centers in the hypothalamus causes the release of antidluretic hormone (ADH) from the posterior pituitary. Release of ADH results In the formation of less urine, thereby conserving body water. The urine formed appears more concentrated, dark, and cloudy than when water intake is adequate. Despite the controls to maintain water balance, several factors can Influence water balance and the requirement for water. [Pg.1116]


See other pages where Thirst center is mentioned: [Pg.339]    [Pg.625]    [Pg.238]    [Pg.219]    [Pg.2463]    [Pg.851]    [Pg.1992]    [Pg.930]    [Pg.758]    [Pg.117]   
See also in sourсe #XX -- [ Pg.1992 ]




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