ADHafgifte

ADHafgifte refers to the secretion of antidiuretic hormone (ADH), also known as vasopressin, from the posterior pituitary after production in the hypothalamus. It is a central component of body water homeostasis and blood pressure regulation.

ADH is released in response to rising plasma osmolality, detected by hypothalamic osmoreceptors, and to decreases in effective circulating blood volume or pressure, sensed by baroreceptors. Small changes in osmolality can trigger substantial changes in ADH release. Other stimuli include pain, nausea, stress, and certain medications.

In the kidney, ADH binds to V2 receptors on the collecting duct cells, promoting the insertion of aquaporin-2 water channels into the apical membrane. This increases water reabsorption, concentrates the urine, and reduces urine volume. ADH can also act on V1 receptors in vascular smooth muscle, contributing to vasoconstriction and, in some conditions, raised blood pressure.

Disorders of ADHafgifte include hyponatremia caused by excessive ADH secretion (syndrome of inappropriate ADH secretion, SIADH) and disorders of ADH production or action such as central diabetes insipidus (deficient ADH) or nephrogenic diabetes insipidus (kidneys unresponsive to ADH). Pregnancy and certain drugs can modify ADH dynamics.

Diagnosis typically involves measuring serum and urine osmolality and sodium; copeptin can serve as a surrogate marker for ADH. Treatment is disorder-specific: SIADH is often managed with fluid restriction and, when appropriate, vasopressin receptor antagonists; central DI is treated with desmopressin; nephrogenic DI focuses on underlying causes and may include specific pharmacologic strategies.