Summary
Highlights
The neurohypophysis is part of the total hypophysis, located in the sella turcica. It's a neuroectodermal tissue, an extension from the hypothalamus where neuronal cell bodies producing neurohypophyseal hormones (oxytocin and ADH) are located in the paraventricular and supraoptic nuclei. These neurons project axons through the infundibular stalk to the posterior pituitary. The neurohypophysis is distinct in origin from the anterior hypophysis.
The neurohypophysis includes nerve terminals of magnocellular neurons from the paraventricular and supraoptic nuclei, pituicytes (glial-like cells with contractile capacity), and perivascular elements. The key hormones are arginine vasopressin (ADH) and oxytocin, both encoded on chromosome 20. They are synthesized in the hypothalamus and transported to the posterior pituitary, bound non-covalently to neurophysins (neurophysin 2 for ADH and neurophysin 1 for oxytocin). Neurophysins prevent degradation during axonal transport. The synthesis ratio of ADH to oxytocin is 4:1.
ADH and oxytocin are peptide hormones with similar structures, differing by only two amino acids, which significantly changes their function. Release occurs when a stimulus depolarizes the neuronal cell body, propagating an action potential to the presynaptic terminal in the posterior pituitary. This increases presynaptic calcium, leading to exocytosis of vesicles containing the hormones into the capillaries. Pituicytes play a role by retracting during stimulation, increasing the contact surface between nerve terminals and capillaries, thereby facilitating hormone release.
ADH secretion is primarily stimulated by changes in plasma osmolarity. Osmoreceptors in the hypothalamus detect increases in extracellular fluid osmolarity, leading to dehydration and activation of ADH-producing neurons. ADH acts on the kidneys to reabsorb free water, decreasing diuresis and increasing extracellular fluid volume. This lowers plasma osmolarity, completing a negative feedback loop. The sensitivity to osmolarity changes is high; a 1% change can significantly alter ADH levels.
Baroreceptors also influence ADH secretion. A decrease in arterial blood pressure or plasma volume (e.g., from hemorrhage) stimulates ADH release, increasing water reabsorption and blood volume. Conversely, conditions like microgravity or the Trendelenburg position, which increase blood flow to baroreceptors, decrease ADH. Oro-pharyngeal receptors can inhibit ADH release quickly upon water intake, anticipating systemic changes. Stress, exercise, pain, hypoglycemia, and hypoxia stimulate ADH, while cold, hypoosmolarity, and alcohol inhibit it.
ADH has antidiuretic effects via V2 receptors in kidney tubules, increasing water permeability by incorporating aquaporins, reducing urine flow. It also has vasoconstrictive effects via V1 receptors (hence 'vasopressin'). ADH can stimulate ACTH production from corticotrophs. Other actions include increasing capillary permeability to urea in the kidney, stimulating gastrointestinal motility, and decreasing gastric, salivary, and pancreatic secretions. ADH also influences memory, learning, sexual receptivity, and maternal behavior through its actions in other brain regions.
Oxytocin secretion is triggered by neural reflexes. Suckling stimulates oxytocin release via thoracic nerves. Uterine cervical and vaginal dilation during childbirth (Ferguson reflex) also activate oxytocin release via pelvic nerves. Sexual intercourse can similarly stimulate it. These segmental nerve pathways signal the supraoptic and paraventricular nuclei to produce oxytocin. Stress can inhibit oxytocin release, impacting processes like lactation. Estrogens and noradrenaline (via alpha receptors) stimulate oxytocin, while noradrenaline (via beta receptors), progesterone, and opiates inhibit it. Non-suckling stimuli, like a baby's cry, can also trigger oxytocin release, anticipating the need for lactation.
Oxytocin primarily causes contraction of smooth muscle. In the mammary gland, it contracts myoepithelial cells for milk ejection. In the uterus, it causes strong contractions crucial for childbirth, a process potentiated by estrogen and antagonized by progesterone. It also aids ovulation by contracting smooth muscle fibers around ovarian follicles. In males, oxytocin contributes to the contraction of the male genital tract, facilitating ejaculation. It can decrease testosterone and stimulate prolactin secretion. Oxytocin also plays a role in maternal bonding and facilitating the 'forgetting' of birth pain.