Vasopressin (ADH)
Posterior Pituitary Hormones

Author: Gianpiero Pescarmona
Date: 26/02/2012



Vasopressin is a neurohypophysial hormone found in most mammals. It is a nonapeptide with a cyclical structure.


Vasopressin is codified by a gene contained into the 20th human chromosome.

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When relevant for the function

  • Primary structure The amino acid sequence is characterized by a sulphide bridge between two cysteines.
  • Secondary structure
  • Tertiary structure
  • Quaternary structure

Protein Aminoacids Percentage
The Protein Aminoacids Percentage gives useful information on the local environment and the metabolic status of the cell (starvation, lack of essential AA, hypoxia)

Protein Aminoacids Percentage (Width 700 px)


The ADH is synthesized into the sopraoptic and paraventricular nucleus (SON and PVN) by specialized nerve cells that reside into the hypothalamus and from which slope, through pituitary peduncle, hypothalamic nerve cells until reaching neurohypophisis from which ADH is released as a consequence of a specific stimulus.

The ADH synthesis is formed by six main passages:

1. Translation of mRNA into a pre-pro-hormone of 166 amino acids into the ribosome of cellular master neuron of SON;
2. Removal of the signalling peptide while the peptide is still anchored to the ribosomes and formation of the pro-hormone;
3. Glycosylation into the Golgi apparatus and gathering into neuro secretor granules;
4. Transfer along the sopraoptic part as osmotically inactive granules;
5. Gathering into the back hypophisys and become a nonapeptide into the granules; the granules are conserved in two pools, one quickly available, closed to the cell membrane, and the other far away, as a reserve.
6. Following the membrane depolarization, the quickly available granules are melted with the cell membrane and move to the extracellular space and then into bloodstream where the ADH permeate the peripheral and glomerular capillaries.

mRNA synthesis

Its mRNA is very selectively expressed in hypothalamus

protein synthesis

post-translational modifications



ADH influences the following factors:
KIDNEY -> Vasopressin has a role into the convoluted tubule where promotes the insertion, into the apical membrane of epithelial tubular cells, of aquaporine (a type of proteins). Vasopressin binds specific receptors paired up with stimulatory G protein (so-called V2) placed on basolateral membrane. Stimulatory G proteins activate adenylyl cyclise which allows cAMP and pyrophosphate formation starting from ATP. cAMP activates PKA that phosphorylates vesicles containing aquaporine in order to insert them into the plasmatic membrane. In the event of decline of vasopressin level aquaporine will be internalised into the cell through endocytosis. The aquaporine insertion into the epithelial tubular cells’ apical membrane makes it more permeable to water and as a consequence increases the permeability to water of all the renal tubule, due to the effect of ADH on aquaporines’ exposition.
Moreover, vasopressin raises urea’s permeability in collecting ducts, determining an increased urea’s reabsorption in the renal medulla. Urea does not constitute a stimulus for the inhibition of vasopressin release.
Another important function of this hormone is stimulating sodium reabsorption in the ascending portion of the loop of Henle.

CARDIOVASCULAR SYSTEM -> Vasopressin, by raising the total peripheral resistances, causes an increase of blood pressure. ADH binds to V1 receptors on vascular smooth muscle to cause vasoconstriction via the IP3 signal trasduction pathway: vasopressin activates phospholipase C (PL-C) that causes IP3 and diacylglycerol (DAG) formation from PIP2 . The IP 3 then stimulates the sarcoplasmic reticulum (SR) to release calcium. The formation of DAG activates protein kinase C (PK-C), which can also contribute to vascular smooth muscle contraction via protein phosphorylation. This way ADH induces contraction of smooth musculature and veins and so increases arterial pressure. Furthermore vasopressin raises factor VIII levels, probably through stimulation of its release by vascular endothelium, and stimulates platelets gathering.

cellular localization,
biological function

  • Enzymes
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  • Cell signaling and Ligand transport
  • Structural proteins


The membrane depolarisation, and so the ADH secretion stimulus, is regulated by four different mechanisms:
1. Hypothalamic osmoceptors: those specialized cell groups are closed to the SON and PVN. There is at least one synapsis between the hypothalamic receptors and the SON and PVN magnocellular neurons. Acetylcholine is the neuromediator which binds to nicotine receptors. Osmoceptors are sensible to changes in the osmotic pressure and so, based on the variations of salt concentration, are activated and will stimulate the neurohypophysis.
2. Modification to the circulating volume: receptors in charge of this system are into the left atrium. The paths followed are those of the ascending vagal segment that in normal conditions are constantly inhibiting with the same strength the ADH secretion. When the atrial volume is reduced, the inhibitory tone is removed and the ADH is secreted in quantities 100 times bigger than the increase started by osmoceptors’ stimulation. Moreover, the volume sensors are far less accurate than the osmoceptors. The reduction of the atrial volume must be of 10% in order to activate the secretion.
3. Activation of the carotid baroceptors: ADH secretion activated by this process is around 500 times bigger than the one started by osmoceptors and causes a massive vasoconstriction. Impulses coming from baroceptors run through IX and X cranial nerve, up to nucleus contained into the bulb (nucleus of the solitary tract, NTS) and through the mid-brain, reach hypothalamus sopraoptic nucleus along adrenergic ways. Considering that pressoceptors are normally tonic inhibitor of ADH release, a reduction of hematic volume and arterial pressure lowers the flow of inhibiting impulses, causing ADH secretion.
4. Finally, ADH secretion is negatively regulated by an oropharyngeal reflex: water ingestion blocks ADH secretion before the modification of plasmatic osmolality values.


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