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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 Hypovolemia/Hypotension 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 Legend: Pathophysiology Mechanism Sign/Symptom/Lab Finding Complications Published May 20, 2023 on www.thecalgaryguide.com