CONTROL OF PLASMA OSMOLALITY
Plasma osmolality is closely regulated by osmo-receptors in the hypothalamus. These specialized neurons control both the secretion of antidiuretic hormone (ADH) and the thirst mechanism. Plasma osmolality is therefore maintained within relatively narrow limits by varying both water intake and water excretion.
Specialized neurons in the supraoptic and paraven-tricular nuclei of the hypothalamus are very sensi-tive to changes in extracellular osmolality. When ECF osmolality increases, these cells shrink and release ADH from the posterior pituitary. ADH markedly increases water reabsorption in renal collecting tubules , which tends to reduce plasma osmolality back to normal. Con-versely, a decrease in extracellular osmolality causes osmoreceptors to swell and suppresses the release of ADH. Decreased ADH secretion allows a water diuresis, which tends to increase osmolality to nor-mal. Peak diuresis occurs once circulating ADH is metabolized (90–120 min). With complete suppres-sion of ADH secretion, the kidneys can excrete up to 10–20 L of water per day.
The carotid baroreceptors and probably atrial stretch receptors can also stimulate ADH release following a 5–10% decrease in blood volume. Other nonosmotic stimuli include pain, emotional stress, and hypoxia.
Osmoreceptors in the lateral preoptic area of the hypothalamus are also very sensitive to changes in extracellular osmolality. Activation of these neurons by increases in ECF osmolality induces thirst and causes the individual to drink water. Conversely, hypoosmolality suppresses thirst. Thirst is the major defense mechanism against hyperosmolality and hypernatremia, because it is the only mechanism that increases water intake.