The volume of ECF is determined primarily by the total amount of osmotically active solute in the ECF. Excessive loss of Na+ in the stools (diarrhea), urine (severe acidosis, adrenal insufficiency), or sweat (heat prostration) decreases ECF volume markedly and eventually leads to shock.
The regular of extracellular fluids is based on vasopressin (ADH) and renin-angiotensin system. The homeostatic mechanisms for controlling blood volume are focused on controlling sodium balance. In contrast, the homeostatic mechanisms for controlling plasma osmolality, which is largely determined by serum sodium concentration, are focused on controlling water balance.
The extracellular and intracellular concentration of sodium and potassium are maintained by Na+-K+-ATPase (although solutes generally cannot freely cross cell membranes) and these maintained concentration determine the osmolality of extracellular and intracellular fluids. Most cell membranes are freely permeable to water, and thus the osmolality of intra- and extracellular body fluids is the same. Otherwise, water will move from the hypotonic compartments to hypertonic compartments.
The Genesis of Osmosis
When a substance is dissolved in water, the concentration of water molecules in the solution is less than that in pure water, because the addition of solute to water results in a solution that occupies a greater volume than dose the water alone. If the solution is placed on one side of a membrane that is permeable to water but not to the solute, and an equal volume of water is placed on the other, water molecules diffuse down their concentration (chemical) gradient into the solution. This process – the diffusion of solvent molecules into a region in which the membrane is impermeable – is called osmosis.
The tendency for movement of solvent molecules to a region of greater solute concentration can be prevented by applying pressure to the more concentrated solution. The pressure necessary to prevent solvent migration is the osmotic pressure of the solution. Just like shown in picture below.
Control of Vasopressin Secretion
Plasma osmolality and ECF volume can affect the secretion of ADH.
ADH increases the permeability of the collecting ducts of the kidney, so that more water enters the hypertonic interstitium of the renal pyramids and the urine becomes concentrated and its volume decreases (the hypertonic status of renal pyramid interstitium is caused by the “countercurrent mechanism”. The thin descending limb is only permeable to water. And the thick ascending limb has active transport of Na+ and Cl–which makes the intersitium hypertonic).
The overall effect of ADH is retention of water in excess of solute; consequently, the effective osmotic pressure of the body fluids is decreased. In the absence of vasopressin, the urine is hypotonic to plasma, urine volume is increased, and there is a net water loss; consequently, the osmolality of the body fluid rises.
The secretion of ADH is controlled by mechanisms of osmotic stimuli and volume feedback effect.
When effective osmotic pressure of the plasma is increased above 285 mOsm/kg, the rate of discharge of neurons containing vasopressin increases and vasopressin secretion occurs. Generally, at 285 mOsm/kg, plasma vasopressin is at or near the limits of detection by available assays.
Meanwhile, as plasma osmolality increases, the feeling of thirst gets stronger and people will take more water. The osmotic threshold for thirst is the same as or slightly greater than the threshold for increased vasopressin secretion.
A decreased extracellular volume or major decrease in arterial pressure reflexively activates increased ADH secretion. To say strictly, the effective circulating blood volume affeccts ADH secretion via volume receptors. These receptors are located in low- and high-pressure portions of the vascular system. The response is mediated by neural pathways originating in cardiopulmonary baroreceptors, and if arterial pressure decreases, from arterial baroreceptors. There is an inverse relationship between the rate of ADH secretion and the rate of discharge in afferents from stretch receptors. AngII reinforces the response to hypovolemia and hypotension by acting on the circumventricular organs to increase ADH secretion (but it is not certain which of the circumventricular organs are responsible for the increases in ADH secretion).
Also, volume effects have an inverse relationship with the feeling of thirst (probably by the increased level of ang II).
Some other factors such as pain, nausea, surgical stress, and emotions would affect the secretion of ADH. Alcohol decreases ADH secretion.
Control of Renin-Angiotensin System
The most important angiotensin is ang II. In physiology,
angiotensin II produces arteriolar constriction and a rise in systolic and diastolic blood pressure.
Ang II also acts directly on the adrenal cortex to increase the secretion of aldosterone.
Besides, ang II acts on the brain to decrease the sensitivity of the baroreflex, which potentiates the pressor effect of ang II.
Ang II acts on the brain to increase water intake and increase the secretion of ADH.
In general, four factors regulate the secretion of rennin and the resultant ang II and aldosterone. When arteriolar pressure at the level of the JG cells falls, renin secretion is enhanced. Renin secretion is inversely proportional to the amount of Na+ and Cl– entering the distal renal tubules from the loop of Henle. Besides, ang II fees back to inhibit renin secretion by a direct action on the JG cells. Finally, increased activity of the sympathetic nervous system increases renin secretion.
Additional Information (updated on Jun 12th 2014)
Water intake is increased by increased effective osmotic pressure of the plasma and by decrease in ECF volume (to say strictly, the effective circulating blood volume) and the impact of effective circulating blood volume >the one of effective osmotic pressure (and the Plasma Osmolality – ADH Secretion cluve shifts to the left by decreased effective circulating blood volume).
Osmolality acts via osmoreceptors, receptors that sense the osmolality of the body fluids (more accurately, the plasma). These osmoreceptors are located in the anterior hypothalamus. Decrease in ECF volume stimulate thirst by a pathway independent of that mediating thirst in response to increased plasma osmolality. Generally, the effect of ECF volume depletion on thirst is mediated in part via the rennin-angiotensin system. The angII acts on the subfornical organ (one of the circumventricular organs of the brain), a specialized receptor area in the diencephalon, to stimulate the neural area concerned with thirst. Some evidence suggests that it acts on the OVLT (no BBB) as well.
However, drugs that block the action of angII do not completely block the thirst response to hypovolemia (and decreased effective circulatory pressure).