8th February 2024

Collecting ducts

Within the collecting duct, urine concentration is controlled by levels of antidiuretic hormone (ADH) within the blood. Osmoreceptors within the hypothalamus detect changes in osmotic pressure, i.e. blood volume. Raised pressures activate the osmoreceptors, activating neurosecretory cells within the hypothalamus to produce ADH. ADH is released from the posterior pituitary to the bloodstream. Conversely, low osmotic pressure inhibits osmoreceptors and, thus, ADH production and secretion. ADH travels within the blood to the kidney and then binds to receptors in the collecting duct, stimulating the insertion of aquaporin water channels into the luminal membrane. Water can then move out of the collecting duct, resulting in decreased urine concentration and increased water return to the blood. ADH also prevents water loss through sweating and causes arteriole constriction, increasing blood pressure.

In periods of fluid overload, atrial stretch releases atrial natriuretic peptide from the atria (ANP). This inhibits the adrenal release of aldosterone, reducing sodium reabsorption and pituitary release of ADH, preventing water reabsorption. The overall effect is an increased diuresis. 

Drugs can interfere with ADH activity in several ways. An example of this is alcohol, which inhibits the secretion of ADH, thus increasing urine volume. A further example is lithium, which can cause nephrogenic diabetes insipidus by inhibiting the collecting duct response to ADH, reducing aquaporin channels, and triggering increased urine output. 

Other functions of the collecting duct include a small amount of sodium reabsorption via aldosterone-activated sodium channels and hydrogen ion secretion.