The main sensors that are involved in control of water balance in the body are:
The osmoreceptors are specialised cells in the hypothalamus which respond to changes in extracellular tonicity (rather then to changes in osmolality). The exact mechanism involved is not known but it may be that changes in cell volume affect the concentration of certain critical intracellular molecules or affect the activity of ion channels in the cell membrane.
As Na+ (and its obligatory associated anions - mostly Cl-, HCO3- & protein-) account for 92% of ECF tonicity, these receptors (during normal physiology) function essentially as monitors of ECF [Na+]. These receptors have been called ‘osmo-sodium’ receptors. This is not strictly correct as the variable directly sensed is tonicity and this can change independently of [Na+] in certain non-physiological situations (eg mannitol infusion); but in nearly all physiological circumstances it is a functionally accurate statement.
They respond to a change as small as a 1 to 2% increase in tonicity. Water intake can vary greatly but plasma osmolality varies only one to two percent because of the efficient and powerful control system coupled to these osmoreceptors.
These receptors are monitoring 'water balance' indirectly because they look at the effect of an excess or deficit of water by its effect on tonicity. This could cause a problem, if for example, both ECF water and solute increased together so that [Na+] and tonicity remained constant. This is what happens with an intravenous infusion of normal saline (ie an isotonic expansion of the ECF). Fortunately the body has several mechanisms of recognising changes in intravascular volume. This is the role of the baroreceptors.
Note that the osmoreceptors effectively respond to the ECF [Na+] and this is also the factor which effectively controls the distribution of water between intracellular and extracellular fluid. (See Section 6.1) The ECF [Na+] thus sets the ECF volume and controls the ICF:ECF distribution of body water so it necessarily follows that:
Effective intravascular volume can be independently assessed by the low pressure baroreceptors (volume receptors) which also provide input to the hypothalamus. These volume receptors are located in the right atria and great veins and respond to the transmural pressure in the the walls of these vessels.
The threshold of the volume receptors for causing changes in ADH secretion is an 8 to 10% change in blood volume. But when stimulated they cause ADH levels to be much higher than that seem with osmoreceptor stimulation.
Hypovolaemia is a more potent stimulus for ADH release than is hyperosmolality. A hypovolaemic stimulus to ADH secretion will override a hypotonic inhibition and volume will be conserved at the expense of tonicity. The maximum levels of ADH reached with a significant (20%) volume depletion is about 40pg/ml which is larger than the 12-15pg/ml reached with a maximum isovolaemic increase in osmolality.
The high pressure baroreceptors input to the hypothalamus via adrenergic pathways. These baroreceptors are located in the carotid sinus and respond to changes in mean arterial blood pressure. The input to the hypothalamus from the volume receptors and the high pressure baroreceptors rarely conflicts as hypovolaemia tends to be associated with hypotension (and vice versa).
In addition to changes in intravascular volume, there are several other non-osmotic factors which affect ADH secretion. These include input from higher cerebral centres and various drugs.