The posterior pituitary gland stores and releases two small peptide neurohormones: Antidiuretic Hormone (ADH), also known as vasopressin, and Oxytocin. These hormones are produced by specialized nerve cells in the hypothalamus. When a stimulus is received, these nerve cells trigger an electrical signal that travels to the posterior pituitary, prompting the near-instantaneous release of the stored hormones directly into the bloodstream.
Anatomy: The Hypothalamus-Pituitary Connection
The connection between the hypothalamus and the posterior pituitary is a direct neural pathway, unlike the blood vessel-based connection of the anterior pituitary. The cell bodies synthesizing these hormones are clustered in two distinct hypothalamic areas: the supraoptic nucleus (SON) and the paraventricular nucleus (PVN). ADH is primarily synthesized in the SON, while Oxytocin is mainly produced in the PVN.
These specialized nerve cells, called magnocellular neurons, extend long axons that form the hypothalamic-hypophyseal tract. This tract carries the newly synthesized hormones into the posterior pituitary gland. The hormones are packaged inside vesicles, transported down the axons, and stored near the nerve endings in structures called Herring bodies.
The posterior pituitary (neurohypophysis) functions as a terminal for these nerve cells. The hormones remain stored in these nerve endings, ready for rapid release upon receipt of an electrical signal from the hypothalamus. This arrangement allows for a swift, nervous system-driven response.
The Specific Stimuli for ADH Release
ADH release is governed by the body’s need to conserve water and maintain fluid balance, responding to two main physiological changes. The most sensitive trigger is an increase in plasma osmolarity (solute concentration in the blood). Specialized osmoreceptors in the hypothalamus detect even a slight increase, signaling the onset of dehydration.
This hyperosmolar state activates the ADH-producing neurons in the supraoptic nucleus. The resulting ADH surge acts on the kidneys to increase water reabsorption, helping to dilute the blood and restore normal osmolarity.
A second, more forceful trigger for ADH release is a significant drop in blood volume or blood pressure. Baroreceptors (pressure sensors) in major blood vessels and the heart detect a substantial decrease, typically 10% or more. This signal is transmitted to the hypothalamus, overriding the osmotic signal and causing a massive release of ADH. High concentrations of ADH act as a potent vasoconstrictor to raise blood pressure, in addition to retaining water in the kidneys.
The Specific Stimuli for Oxytocin Release
Oxytocin release is triggered by specific sensory and neural reflexes associated with reproductive functions and physical touch. The two most significant triggers involve powerful positive feedback loops.
Milk Ejection Reflex
The first trigger is the milk ejection reflex, stimulated by the mechanical sensation of suckling on the nipple. Sensory nerves send signals to the hypothalamus’s paraventricular nucleus. This neural input causes a pulsatile release of oxytocin, which travels to the breast tissue to contract myoepithelial cells and eject milk. Conditioned responses, such as a baby’s cry, can also trigger release before physical suckling begins.
Ferguson Reflex
The second major trigger is the Ferguson reflex, which drives labor and childbirth. As the baby moves down the birth canal, mechanical stretching of the cervix and vagina sends strong neural signals to the hypothalamus. The hypothalamus releases a burst of oxytocin, stimulating uterine muscles to contract. These contractions increase cervical stretching, signaling for more oxytocin release, creating a positive feedback cycle until delivery is complete.
The Release Mechanism: From Electrical Signal to Hormone Dump
The final step in the release of ADH or Oxytocin follows an identical cellular process, regardless of the initial stimulus. The stimulus generates an electrical signal (action potential) originating in the hypothalamic nerve cell body. This action potential travels the length of the axon down to the nerve terminal in the posterior pituitary.
When the action potential reaches the nerve terminal, it changes the electrical charge of the cell membrane. This change immediately triggers the opening of specialized voltage-gated calcium channels. Calcium ions, which are concentrated outside the cell, rush into the nerve terminal.
The influx of calcium acts as the final chemical signal, triggering exocytosis. Calcium causes the hormone-filled vesicles (containing ADH or Oxytocin) to fuse with the nerve terminal’s outer cell membrane. Once fused, the contents are expelled directly into the surrounding capillary bed, allowing the neurohormone to enter the systemic circulation.