ADH and Water Balance Regulation

Antidiuretic hormone (ADH), also called vasopressin, determines how much water the kidneys return to the circulation. It is made in the hypothalamus, stored in the posterior pituitary, and released when plasma becomes more concentrated or when effective circulating volume falls. ADH acts mainly at V2 receptors in the renal collecting ducts. It inserts aquaporin water channels into the tubular membrane, allowing water to move from urine back into the bloodstream. Urine becomes concentrated and urine volume falls. ADH does not directly retain sodium; it retains water. That distinction explains why excessive ADH can lower the measured serum sodium concentration by dilution. Osmoreceptors respond to small rises in plasma osmolality, while baroreceptors respond to a larger threat: inadequate arterial filling. Hemorrhage, vomiting, diarrhea, heart failure, cirrhosis, and shock can all trigger ADH release even when serum osmolality is low. From the body’s perspective, preserving perfusion takes priority over maintaining a normal sodium concentration. Thirst works alongside ADH. ADH reduces renal water loss; thirst drives water intake. When both mechanisms are intact, water balance is usually maintained. Problems develop when ADH secretion...