• The posterior pituitary gland releases two hormones:
  • Anti-diuretic hormone (Vasopressin)
  • Oxytocin
• The precursors of these hormones are produced in the hypothalamic magnocellular neurons (supraoptic and paraventricular nuclei). Afterwards, they are packed into secretory granules. These granules migrate along the neural axons into the posterior pituitary.

Anti-diuretic hormone (Vasopressin).

• Vasopressin, also known as the antidiuretic hormone (ADH), plays a crucial role in maintaining water balance. It does this by regulating water absorption in the kidneys. Without ADH, the kidney's collecting duct cells are impermeable to water, leading to water loss in urine. However, when ADH is present, water can osmotically move across the collecting duct cells.

• ADH is synthesized mainly in the hypothalamus, specifically in the supraoptic nucleus (SO), and also in the paraventricular nucleus (PVN). It is stored and released from the posterior pituitary.

• ADH is a significant controller of water excretion, extracellular fluid (ECF) volume, and osmolarity.

• It activates G protein-coupled V2 receptors, which allow the transposition of aquaporin 2 from their intracellular locations to the luminal cell membrane. Here, aquaporin serves as a water channel, allowing water to pass through.

• In circumstances of severe hemorrhage, high levels of ADH activate V1 receptors on vascular smooth muscle, causing vasoconstriction.

• The activation of V1 receptors increases intracellular calcium, leading to intense vasoconstriction that elevates the arterial blood pressure in cases of hemorrhage. (vasopressor effect). This effect is minor, since reinin-angiotensin & sympathetic nervous systems are the primary regulators of arterial BP.

• Osmoreceptors are neurons that react to increased plasma osmolarity, primarily sodium concentration. These receptors stimulate the supraoptic nucleus (SO) and paraventricular nucleus (PVN) to secrete Antidiuretic Hormone (ADH) from the posterior pituitary. Additionally, they prompt water consumption through hypothalamic centers that regulate thirst.

• The SO and PVN also receive input from atrial volume receptors and arterial receptors. High blood volume or blood pressure generally inhibits ADH secretion.

• While ADH secretion is most sensitive to plasma osmolarity, if blood volume decreases—such as in cases of hemorrhage or cardiac output failure—high levels of ADH are secreted, even if it leads to abnormal plasma osmolarity.

Regulation of ECF volume and osmolarity.

1. Volume Regulation: A decrease in volume prompts an increase in ADH, while an increase in volume prompts a decrease in ADH. Stimuli from stretch receptors act to chronically inhibit ADH secretion. A decrease in blood volume causes these receptors to send fewer signals to the CNS, reducing the chronic inhibition of ADH secretion. This mechanism is particularly crucial for restoring ECF volume after a hemorrhage.
2. Osmoregulation: An increase in osmolarity (concentration of solutes in the blood) prompts an increase in ADH, while a decrease in osmolarity prompts a decrease in ADH. A 1% increase in the osmolarity of the ECF bathing the hypothalamic osmoreceptors will trigger an increased rate of ADH secretion. Conversely, a similar decrease in osmolality will decrease ADH secretion. This mechanism keeps the ECF osmolality very close to 285 mOsm/L.

• Antidiuretic hormone formation begins in the supraoptic nuclei, and oxytocin production starts in the paraventricular nuclei. Once translated, these hormones are packaged into neurosecretory vesicles and transported to the posterior pituitary in association with intra vesicular proteins known as neurophysins.