Antidiuretic hormone
| Vasopressin; Adiuretine | ||
|---|---|---|
|
||
| Dome model | ||
| Properties of human protein | ||
| Mass / length primary structure | 9 amino acids; 1084 daltons | |
| Identifier | ||
| Gene names | AVP ; ADH; AVP-NPII; VP | |
| External IDs | ||
| Drug information | ||
| ATC code | H01 BA01 | |
| DrugBank | DB00067 | |
| Drug class | Vasoconstrictor | |
| Orthologue | ||
| human | House mouse | |
| Entrez | 551 | 11998 |
| Ensemble | ENSG00000101200 | ENSMUSG00000037727 |
| UniProt | P01185 | P35455 |
| Refseq (mRNA) | NM_000490 | NM_009732 |
| Refseq (protein) | NP_000481 | NP_033862 |
| Gene locus | Chr 20: 3.08 - 3.08 Mb | Chr 2: 130.58 - 130.58 Mb |
| PubMed search | 551 |
11998
|
The antidiuretic hormone ( ADH ), also known as adiuretin , vasopressin ( INN ) or arginine-vasopressin ( AVP ), is a peptide hormone . It is formed in the brain (in the hypothalamus ) and released from its reservoir (the posterior pituitary lobe ) from a common prohormone together with neurophysin II and copeptin ( CT-proAVP ) . As an "antidiuretic" hormone, it works to preserve body fluids. The name vasopressin refers to its vasoconstricting effect at higher doses (from Latin vas = (blood) vessel and Latin pressus = pressure ).
structure
The primary structure of human ADH consists of nine amino acids . The ADH has an intramolecular disulfide bond and an amidated C-terminus .
production
ADH is produced by nerve cells in the hypothalamus ( nucleus supraopticus and nucleus paraventricularis ), stored in the posterior lobe of the pituitary gland and from there released into the blood as needed. The hypothalamus and the posterior pituitary are parts of the diencephalon . ADH arises from a 143 amino acid long prohormone from which neurophysin II and copeptin also originate, both of which presumably play a role in the transport of ADH.
physiology
ADH causes increased recovery of water from the primary urine through the renal tubules, which concentrates the urine and decreases its volume . This is known as tubular reabsorption . Since the hormone is mainly excreted at night, it enables healthy adults to sleep through the night without bedwetting .
ADH works in two main ways:
- Peripheral effect: ADH is transported axonally from magnocellular neurons along the pituitary stalk (tractus supraopticohypophysialis), stored in vesicles of the posterior pituitary gland (also called neurohypophysis ) and, if required, released into the blood , where the osmolality of the blood is reabsorbed in physiological concentrations by water reabsorption in the kidney regulated by V2 receptors. In various diseases such as infections, shock or trauma, higher concentrations increase blood pressure via so-called V1 receptors in the arteries.
- Central effect: ADH is secreted from so-called parvocellular neurons into the pituitary portal circulation, via which it reaches the anterior pituitary lobe (also called adenohypophysis ). From this anterior pituitary lobe it is in turn secreted into the blood via V3 receptors together with CRH ACTH . ACTH releases cortisol from the adrenal cortex . ADH is therefore part of the body's hormonal stress mechanism.
ADH helps the organism to control the water balance. If there is a lack of water in the organism, the blood plasma becomes hypertonic . This is detected by the osmoreceptors in the hypothalamus , which in turn trigger the release of ADH from the neurohypophysis . Another stimulus for the release of ADH is a lack of volume in the arterial and venous systems, which is registered via baroreceptors in the right atrium of the heart and in the aortic arch . ADH is transported to the collecting duct epithelial cells in the kidney via the blood. Without the influence of ADH, these cells are not permeable to water and thus prevent the reabsorption of water from the primary urine. ADH now couples to membrane-bound V2 receptors which, via cAMP, lead to increased translation of aquaporins (AQP2) and fuse vesicles containing aquaporin with the cell membrane. The aquaporins make the cell membrane temporarily permeable to urea and water, which is osmotically drawn from the primary urine into the hyperosmolar kidney tissue, from which it ultimately returns to the blood. In the kidneys, ADH causes increased reabsorption of water and urea from the urine in the collecting pipes .
The antidiuretic hormone also has a vasoconstricting effect in high concentrations. Both effects raise blood pressure.
Normal values
Measuring ADH is difficult and only a few specialized laboratories offer it. Since the half-life of the analyte is a few minutes, the blood sample must be processed quickly. In addition, ADH binds strongly to platelets, which makes the measurement even more difficult. For these reasons, unlike other hormones, measuring ADH is not an integral part of clinical routine. There is now an alternative by measuring copeptin , which is formed from the common prohormone together with mature ADH and is much easier to measure.
Since ADH is affected by alcohol, smoking and caffeine, twelve hours before the blood draw an alcohol, nicotine and caffeine must leave and 48 hours before a drug abstinence are observed. The determination is made from at least 4.0 mL, deep-frozen EDTA plasma using radioimmunoassays (RIA).
- Blood:
Normal
values for adults are: 2.9 ± 1.0 pg / ml other data speak of: 2.0 - 8.0 pg / ml -
Osmolality :
Indirect estimation of the serum osmolality with the following formula:- Osmolality [mosmol / kg] = 1.86 × Na + [mmol / l] + glucose [mmol / l] + urea [mmol / l] + 9
or - Osmolality [mosmol / kg] = 2 × (Na + [mmol / l] + K + [mmol / l]) + glucose / 18 [mg / dl] + urea / 6 [mg / dl]
- Osmolality [mosmol / kg] = 1.86 × Na + [mmol / l] + glucose [mmol / l] + urea [mmol / l] + 9
The reference range for serum osmolality is 280-310 mosmol / kg. The values for 24-hour urine are 50–1200 mosmol / kg.
Urine osmolality : after twelve hours of thirst, the urine osmolality corresponds to about three times the serum osmolality or approx. 800–900 mosmol / kg
Pathophysiology
With ADH deficiency there is a strong loss of water, diabetes insipidus centralis . If the V2 receptors on the kidneys are not functioning properly (through mutation or destruction), the same symptoms arise, but one then speaks of diabetes insipidus renalis . The water loss that occurs with these symptoms is up to 20 liters per day. The resulting feeling of thirst is quenched by drinking equivalent amounts of fluids.
In the syndrome of inadequate ADH secretion ( SIADH , syn. Schwartz-Bartter syndrome ), there is reduced water excretion and hyponatremia. This syndrome can occur in lung cancer ( paraneoplastic syndrome ), in which degenerate cells produce hormones, in this case ADH or ADH-like substances.
Alcohol inhibits the secretion of vasopressin (ADH) from the pituitary gland, resulting in increased water excretion. This is one reason for the so-called thirst . Lack of fluids can lead to headaches . In contrast, nicotine leads to increased ADH secretion.
ADH as a drug
Vasopressin is used as a substance that increases blood pressure in patients in shock . The diabetes insipidus centralis can be treated by the administration of ADH. However, the not completely identical analogue desmopressin is used . ADH is used in hemodialysis .
literature
- MA Knepper: Systems biology in physiology: the vasopressin signaling network in kidney. In: American Journal of Physiology - Cell Physiology. Volume 303, number 11, December 2012, pp. C1115 – C1124, doi : 10.1152 / ajpcell.00270.2012 , PMID 22932685 , PMC 3530773 (free full text).
Individual evidence
- ↑ Gaurang P. Mavani, Maria V. DeVita, Michael F. Michelis: A Review of the Nonpressor and Nonantidiuretic Actions of the Hormone Vasopressin. In: Frontiers in Medicine. 2, 2015, doi : 10.3389 / fmed.2015.00019 . PMID 25853137 . PMC 4371647 (free full text).
- ↑ Janet K. Bester-Meredith, Alexandria P. Fancher, Grace E. Mammarella: Vasopressin Proves Essential: Vasopressin and the Modulation of Sensory Processing in Mammals. In: Frontiers in Endocrinology. 6, 2015, doi : 10.3389 / fendo.2015.00005 . PMID 25705203 . PMC 4319160 (free full text).
- ^ Ron Stoop: Neuromodulation by Oxytocin and Vasopressin. In: Neuron. 76, 2012, p. 142, doi : 10.1016 / j.neuron.2012.09.025 . PMID 23040812 .
- ↑ UniProt P01185
- ↑ Ary Serpa Neto, Antônio P Nassar, Sérgio O Cardoso, José A Manetta, Victor GM Pereira, Daniel C Espósito, Maria CT Damasceno, James A Russell: Vasopressin and terlipressin in adult vasodilatory shock: a systematic review and meta-analysis of nine randomized controlled trials. In: Critical Care. 16, 2012, p. R154, doi : 10.1186 / cc11469 . PMID 22889256 . PMC 3580743 (free full text).
- ↑ Seyed Seifollah Beladi Mousavi, Mohamad Reza Tamadon: Vasopressin and Prevention of Hypotension during Hemodialysis. In: Iranian Red Crescent Medical Journal. 16, 2014, doi : 10.5812 / ircmj.20219 .
