Antidiuretic hormone

The secretion of antidiuretic hormone (ADH, also known as vasopressin, Chapter 45) from the posterior pituitary is influenced by the osmolality of body fluids (osmotic), and the volume and pressure of the vascular system (Figure 39.1). Osmotic control of ADH secretion is highly sensitive, with a change of 1% being sufficient to alter ADH release. Shrinkage of osmoreceptor cells located in the anterior hypothalamus (close to supraoptic nuclei) in response to an increase in extracellular fluid osmolality (due to water deficit, for example) leads to nerve signals being sent to hypothalamic ADH-producing neuroendocrine cells (Chapter 45), culminating in the release of ADH from axon termini in the posterior pituitary. At the kidney, ADH interact with V₂ receptors on principal (P) cells, promoting the translocation of aquaporin-2 water channels to the apical membrane, which results in increased water reabsorption and excretion of a small volume of concentrated urine (Figure 39.2). The water conserved dilutes extracellular solutes, thereby correcting the initial hyperosmotic extracellular fluid. The opposite sequence of events occurs with hypo-osmotic extracellular fluid (such as with excess water ingestion).

Haemodynamic control of ADH release involves receptors in low pressure (left atrium and large pulmonary vessels) and high pressure (aortic arch and carotid sinus) regions of the circulation, which detect changes in blood volume and pressure, with afferent signals leading to appropriate control of ADH release to restore blood volume/pressure to normal (Figure 39.1). This is a much less sensitive mechanism than that of osmotic control; change of 5–10% reduction in blood volume is required for plasma ADH levels to change appreciably.

Fluid intake is regulated by the thirst response, the conscious desire to drink water. Neural centres involved in regulating water intake (thirst centre) located in the hypothalamus (in regions similar to those in control of ADH release) respond to a number of stimuli (Figure 39.1). It seems that the ADH and thirst systems work in concert to maintain water balance (Figure a), although with regard to body fluid osmolality, ADH secretion is secreted at a lower threshold than that for thirst. Thus, an increase in plasma osmolality evokes thirst with water ingestion and secretion of ADH with resultant conservation of water, while a fall in plasma osmolality leads to suppressed thirst and a lack of ADH release with enhanced renal water excretion.