Posterior pituitary

Category: endocrine_axis

Overview

Magnocellular neurons in supraoptic + paraventricular nuclei synthesize oxytocin + arginine vasopressin (AVP, ADH), package them in vesicles, and release into the systemic circulation at the posterior pituitary. AVP: V1A (vasoconstriction), V1B (ACTH release), V2 (renal collecting duct aquaporin-2 insertion → water reabsorption). Oxytocin: uterine contraction at parturition + breast myoepithelial milk ejection + social-bonding CNS effects. Therapeutic: oxytocin (IV for labor induction + postpartum hemorrhage); desmopressin (DDAVP — V2-selective for central DI + bedwetting + von Willebrand disease); vasopressin (IV pressor in vasodilatory shock + cardiac arrest historical).

Organ Systems

Pathway Steps

  1. osmotic-or-hypovolemic-stimulus → avp-release — via osmoreceptor + baroreceptor input → magnocellular firing → posterior-pituitary release. Rising plasma osmolality (sensed by hypothalamic osmoreceptors) or falling blood volume triggers the posterior pituitary to release arginine vasopressin (AVP/ADH). Osmotic control is exquisitely sensitive — AVP is the primary defense of water balance and plasma osmolality.
  2. avp-release → renal-water-reabsorption — via V2R → Gs → AQP2 trafficking to apical membrane → water reabsorption. AVP acts on renal collecting-duct V2 receptors to insert aquaporin-2 channels, increasing water reabsorption and concentrating urine. Defects cause diabetes insipidus; desmopressin (a V2 agonist) treats it, while V2 antagonists (tolvaptan) are used for hyponatremia and polycystic kidney disease.

Known Modulators

References