Regulation of Plasma Osmolality

Plasma osmolality is thus the ratio of solutes to water in blood plasma.

Change in osmolality is initiated by either with loss of fluid (volume contraction) or gain of fluid (volume expansion).

The plasma osmolality is maintained within a narrow range by employing mechanisms that regulate both (1) water intake and (2) output.

(1) Regulation of Water Intake

Thirst

Dehydration results in insufficient water in blood and other tissues. The water that leaves the body, as exhaled air, sweat, or urine, is ultimately extracted from blood plasma. As the blood becomes more concentrated, the thirst response is triggered.

Osmoreceptors in the lateral preoptic area of the hypothalamus are very sensitive to changes in extracellular osmolality. These are different from the osmoreceptors that determine ADH secretion. These hypothalamic osmoreceptors, by linking to the cerebral cortex, stimulate thirst when the serum osmolality increases. Thirst occurs with a small increase in the serum osmolality.

The person should (and normally does) respond by drinking water.

Hypoosmolality suppresses thirst. Thirst is the major defense mechanism against hyperosmolality and hypernatremia, because it is the only mechanism that increases water intake.

(2) Regulation of Water Output

Release of Antidiuretic Hormone (ADH)

The hypothalamus of a dehydrated person also releases antidiuretic hormone (ADH) through the posterior pituitary gland. ADH signals the kidneys to recover water from urine, effectively diluting the blood plasma. To conserve water, the hypothalamus of a dehydrated person also sends signals via the sympathetic nervous system to the salivary glands in the mouth. The signals result in a decrease in watery, serous output (and an increase in stickier, thicker mucus output). These changes in secretions result in a “dry mouth” and the sensation of thirst.

Specialized neurons in the supraoptic and paraventricular nuclei of the hypothalamus are very sensitive 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. Circulating ADH binds to its V2 receptors in the collecting duct cells of the kidney, and, via the generation of cyclic adenosine monophosphate, causes insertion of water channels (aquaporin-2) into the renal collecting ducts. This produces increased permeability to water, permitting resorption of water into the hypertonic renal medulla. The end result is that the urine concentration increases and water excretion decreases. Urinary water losses cannot be completely eliminated because there is obligatory excretion of urinary solutes, such as urea and sodium. Conversely, 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 normal. Peak diuresis occurs once circulating ADH is metabolized (90-120 min). With complete suppression of ADH secretion, the kidneys can excrete up to 10-20 L of water per day.

Plasma osmolality is maintained at 285-295 mOsm/kg. ADH responses are detectable with a 1% change in the osmolality.

Nonosmotic Release of Antidiuretic Hormone

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.

 

Fluid Environment of Cells