Physiology of Anti-diuretic hormone

Physiology of Anti-diuretic Hormone (ADH)/Arginine Vasopressin (AVP)
Authors: Manaswi Yerrabattini Reviewers: Parker Lieb Mao Ding Shyla Bharadia Laura Hinz* * MD at time of publication
Limbic activation (e.g., pain, nausea)
Placental production of vasopressinase during pregnancy catalyzes the breakdown of ADH, leading to a temporary Diabetes Insipidus state (see Diabetes Insipidus: Pathogenesis and Clinical Findings slide)
Systemic arteriole vasoconstriction
Hyperosmolar state (i.e., extracellular fluid osmolarity above a certain threshold, most commonly due to hypernatremia)
Sensed by osmoreceptors in hypothalamus
Angiotensin II synthesized through activation of Renin- Angiotensin-Aldosterone System (RAAS) (see Physiology of RAAS slide)
Binds to receptors located in the hypothalamus
↓ pressure sensed by baroreceptors in the heart (left atrium and large veins)
Receptors transmit signals to brain via the vagus nerve
↓ Arterial baroreceptor firing
↑ Sympathetic activity of nerves innervating afferent arterioles
↑ Hypothalamic secretion of ADH (peptide hormone), transportation to posterior pituitary, and release from posterior pituitary into blood circulation
Blood Vessels (Minor role)
Kidneys (Main role)
ADH binds to to Vasopressin-2 receptors on basolateral side of principal cells in kidneys
↑ Insertion of aquaporin II channels onto apical membrane of late distal tubule and collecting ducts
↑ Water reabsorption
↓ Urine Output and Maintains narrow range of serum osmolarity ↑ Urine Osmolarity and preserves sodium homeostasis
ADH binds to Vasopressin-1 receptors on smooth muscle of blood vessels
ADH activates calcium signaling pathway
↑ Blood Pressure
Maintains overall fluid volume status
Sign/Symptom/Lab Finding
Published May 20, 2023 on