ADH is secreted into the blood and acts on V2 receptors in the basal cell membranes of the collecting ducts and distal tubules of the kidney, activating adenylate cyclase, increasing cyclic adenosine monophosphate in their epithelial cells, and phosphorylating aquaporin 2 (AQP2) in the cell membranes, increasing luminal membrane permeability and opening “water channels”, resulting in increased water reabsorption and urine This increases water reabsorption and concentrates urine, producing a significant antidiuretic effect. The abnormal secretion of adrenocorticotropic hormone (ACTH) and antidiuretic hormone (ADH) due to damage to the subthalamic-pituitary system leads to increased urinary sodium excretion, increased water reabsorption by the kidneys, resulting in decreased blood sodium and low blood osmolality, resulting in a series of clinical symptoms of neurological impairment called the syndrome of abnormal secretion of antidiuretic hormone (SIADH). Diagnostic criteria. 1. hyponatremia (blood sodium concentration often below 130 mmol/L); 2. decreased plasma osmolality (often below 270 mOsm/L); 3. increased urinary sodium (>20 mmol/L or >80 mmol/24h, often more than 30 mmol/L); 4. urinary osmolality exceeding plasma osmolality; 5. normal or increased blood volume, normal or decreased plasma creatinine concentration, low uricemia, no edema in peripheral tissues; 6, normal renal, adrenal and thyroid function; 7, water load, unrestricted ADH activity, and improvement after water restriction.