Antidiuretic hormone (ADH), also known as vasopressin, regulates the body’s water content. It helps the kidneys reabsorb water as they filter waste from the blood. Produced in the hypothalamus, ADH is released into the bloodstream from the posterior pituitary gland, maintaining fluid homeostasis.
Understanding the Kidney’s Collecting Ducts
The collecting ducts are the final segments of the nephron, the functional unit of the kidney, where urine is modified. Found in the renal cortex and medulla, they collect filtrate from multiple nephrons and transport it towards the renal pelvis for excretion.
The collecting ducts have variable water permeability. Without hormonal influence, the epithelial cells lining these ducts are largely impermeable to water. However, this permeability can be adjusted to control how concentrated or dilute the final urine becomes. This adjustment is a key factor in the body’s ability to manage its water balance.
The Cellular Mechanism of ADH Action
Antidiuretic hormone increases the water permeability of the collecting ducts through a specific cellular pathway. ADH binds to vasopressin V2 receptors (V2R) on the basolateral membrane of the principal cells within the collecting ducts. These V2 receptors are G-protein coupled receptors.
This binding activates adenylate cyclase, an enzyme that converts adenosine triphosphate (ATP) into cyclic adenosine monophosphate (cAMP). Increased intracellular cAMP levels then activate protein kinase A (PKA). PKA, an enzyme, phosphorylates specific proteins, including aquaporin-2 (AQP2) water channels.
Phosphorylation of AQP2 causes vesicles containing these water channels to translocate from intracellular storage sites to the apical membrane of the collecting duct cells. Once at the membrane, these vesicles fuse, inserting the AQP2 water channels. This insertion increases the number of water channels on the cell surface, enhancing the water permeability of the collecting duct cells.
A medullary osmotic gradient, established by other parts of the nephron like the loop of Henle, is important. This gradient creates a region of higher solute concentration in the interstitial fluid surrounding the collecting ducts in the renal medulla. This osmotic difference provides the driving force for water to move out of the collecting duct lumen, through the inserted AQP2 channels, and into the interstitial fluid.
Impact on Water Balance and Urine Concentration
The increased water permeability in the collecting ducts, a direct result of ADH action, has physiological consequences for the body’s water balance. With more AQP2 channels inserted into the apical membrane, water moves out of the collecting duct lumen. This movement occurs passively, driven by the osmotic gradient, as water flows from an area of lower solute concentration (inside the duct) to an area of higher solute concentration (the interstitial fluid of the renal medulla).
This reabsorbed water returns to the bloodstream, effectively increasing the body’s overall fluid volume. This process directly leads to the formation of concentrated urine, as more water is reclaimed from the filtrate. When ADH levels are high, the kidneys can reabsorb a significant amount of filtered water.
This mechanism is crucial for maintaining the body’s fluid osmolarity and blood volume. By adjusting water reabsorption, ADH helps keep the concentration of solutes in the blood within a narrow, healthy range. When plasma osmolarity increases, indicating dehydration, ADH secretion rises, leading to increased water reabsorption and a return to normal osmolarity. Conversely, when the body is well-hydrated and ADH levels are low, the collecting ducts remain largely impermeable to water, resulting in the excretion of dilute urine.