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Human Body Study

Vasopressin / ADH (Posterior Pituitary)

The vasopressin / ADH pathway Vasopressin is synthesised in PVN/SON of the hypothalamus and released from the posterior pituitary in response to rising plasma osmolality (osmoreceptors) or falling blood volume (baroreceptors). It acts on V2 receptors in the renal collecting duct to reabsorb water via aquaporin-2 channels, and on V1 receptors in vascular smooth muscle to cause vasoconstriction. Restored osmolality and volume close the loop by suppressing further release. ↑ plasma osmolality (osmoreceptors) · ↓ blood volume (baroreceptors) Hypothalamus PVN + SON · magnocellular neurons Posterior pituitary neurosecretory release Kidney collecting duct V2 · aquaporin-2 Vasculature arteriolar smooth muscle V1 · vasoconstriction Water reabsorption concentrated urine Vasoconstriction supports blood pressure axonal transport (neurosecretion) AVP / ADH ↓ osmolality, ↑ volume (−) Osmotic sensitivity is exquisite (1–2% changes); large volume depletion overrides osmolality and forces release. AVP is synthesised in the hypothalamus and merely stored / released by the posterior pituitary.

Signaling chain

Section titled “Signaling chain”

Arginine vasopressin (AVP, antidiuretic hormone) is made in hypothalamic supraoptic and paraventricular nuclei and released from the posterior pituitary. Release is driven by osmoreceptors (sensitive to small rises in plasma osmolality) and baroreceptors (responding to drops in blood volume/pressure). Like oxytocin, it is a neurosecretory pathway, not a classic trophic axis.

Function

Section titled “Function”
  • Water balance — acts on V2 receptors in renal collecting ducts, inserting aquaporin-2 channels to reabsorb free water and concentrate urine.
  • Vascular tone — acts on V1 receptors to cause vasoconstriction, supporting blood pressure during hypovolemia.

Feedback

Section titled “Feedback”

Regulated by plasma osmolality and effective circulating volume. Restored osmolality/volume turns off AVP secretion. Volume depletion can override osmotic control, driving AVP release even when osmolality is low.

Clinical relevance

Section titled “Clinical relevance”
  • Diabetes insipidus — deficiency (central DI) or renal resistance (nephrogenic DI): dilute polyuria, polydipsia, hypernatremia.
  • SIADH — inappropriate excess: water retention and dilutional hyponatremia.
  • Desmopressin (DDAVP) is a V2-selective analog for central DI, enuresis, and some bleeding disorders.

Key labs

Section titled “Key labs”

Serum sodium and osmolality, urine osmolality, copeptin (stable AVP surrogate), water deprivation test.