lypressin

リプレッシン、リプレシン

関

lysine vasopressin

　

WordNet

1. an antidiuretic and vasoconstrictor used to treat diabetes insipidus

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2013/04/18 16:03:03」(JST)

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Arginine vasopressin
Space-filling model of arginine vasopressin
Available structures PDB Ortholog search: PDBe, RCSB List of PDB id codes 1jk4, 1jk6, 1npo, 2bn2
Identifiers
Symbols	AVP; ADH; ARVP; AVP-NPII; AVRP; VP
External IDs	OMIM: 192340 MGI: 88121 HomoloGene: 417 GeneCards: AVP Gene
Gene Ontology Molecular function • protein kinase activity • signal transducer activity • receptor binding • neuropeptide hormone activity • neurohypophyseal hormone activity • V1A vasopressin receptor binding • V1B vasopressin receptor binding • cysteine-type endopeptidase inhibitor activity involved in apoptotic process Cellular component • extracellular region • extracellular space • cytosol • secretory granule • dendrite Biological process • maternal aggressive behavior • positive regulation of systemic arterial blood pressure • generation of precursor metabolites and energy • protein phosphorylation • water transport • signal transduction • elevation of cytosolic calcium ion concentration • cell-cell signaling • negative regulation of female receptivity • grooming behavior • locomotory behavior • positive regulation of cell proliferation • positive regulation of gene expression • positive regulation of glutamate secretion • positive regulation of cell growth • positive regulation of cAMP biosynthetic process • positive regulation of prostaglandin biosynthetic process • positive regulation of cellular pH reduction • positive regulation of peptidyl-serine phosphorylation • response to nicotine • social behavior • regulation of renal sodium excretion • vasoconstriction • hyperosmotic salinity response • maternal behavior • negative regulation of apoptotic process • penile erection • negative regulation of cysteine-type endopeptidase activity involved in apoptotic process • sodium-independent organic anion transport • response to ethanol • positive regulation of vasoconstriction • multicellular organismal water homeostasis • negative regulation of transmission of nerve impulse • transmembrane transport • ERK1 and ERK2 cascade • protein kinase C signaling cascade • negative regulation of release of cytochrome c from mitochondria Sources: Amigo / QuickGO
RNA expression pattern
More reference expression data
Orthologs
Species	Human	Mouse
Entrez	551	11998
Ensembl	ENSG00000101200	ENSMUSG00000037727
UniProt	P01185	P35455
RefSeq (mRNA)	NM_000490	NM_009732
RefSeq (protein)	NP_000481	NP_033862
Location (UCSC)	Chr 20: 3.06 – 3.07 Mb	Chr 2: 130.58 – 130.58 Mb
PubMed search	[1]	[2]

Arginine vasopressin (AVP), also known as vasopressin, argipressin or antidiuretic hormone (ADH), is a neurohypophysial hormone found in most mammals. Its two primary functions are to retain water in the body and to constrict blood vessels. Vasopressin regulates the body's retention of water by acting to increase water absorption in the collecting ducts of the kidney nephron. Vasopressin increases water permeability of the kidney's collecting duct and distal convoluted tubule by inducing translocation of aquaporin-CD water channels in the kidney nephron collecting duct plasma membrane. Vasopressin is a peptide hormone that controls the reabsorption of molecules in the tubules of the kidneys by affecting the tissue's permeability. It also increases peripheral vascular resistance, which in turn increases arterial blood pressure. It plays a key role in homeostasis, by the regulation of water, glucose, and salts in the blood. It is derived from a preprohormone precursor that is synthesized in the hypothalamus and stored in vesicles at the posterior pituitary. Most of it is stored in the posterior pituitary to be released into the bloodstream. However, some AVP may also be released directly into the brain, and accumulating evidence suggests it plays an important role in social behavior, sexual motivation and bonding, and maternal responses to stress.

Physiology

Function

One of the most important roles of AVP is to regulate the body's retention of water; it is released when the body is dehydrated and causes the kidneys to conserve water, thus concentrating the urine and reducing urine volume. At high concentrations, it also raises blood pressure by inducing moderate vasoconstriction. In addition, it has a variety of neurological effects on the brain, having been found, for example, to influence pair-bonding in voles. The high-density distributions of vasopressin receptor AVPr1a in prairie vole ventral forebrain regions have been shown to facilitate and coordinate reward circuits during partner preference formation, critical for pair bond formation.

A very similar substance, lysine vasopressin (LVP) or lypressin, has the same function in pigs and is often used in human therapy.

Kidney

Vasopressin has two effects by which it contributes to increased urine osmolarity (increased concentration) and decreased water excretion. These are:

1. Increasing the water permeability of distal tubule and collecting duct cells in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis. This occurs through insertion of water channels (Aquaporin-2) into the apical membrane of distal tubule and collecting duct epithelial cells. Aquaporins allow water to move down their osmotic gradient and out of the nephron, increasing the amount of water re-absorbed from the filtrate (forming urine) back into the bloodstream.
   V2 receptors, which are G protein-coupled receptors on the basolateral plasma membrane of the epithelial cells, couple to the heterotrimeric G-protein G_s, which activates adenylyl cyclases III and VI to convert ATP into cAMP, plus 2 inorganic phosphates. The rise in cAMP then triggers the insertion of aquaporin-2 water channels by exocytosis of intracellular vesicles, recycling endosomes. Vasopressin also increases the concentration of calcium in the collecting duct cells, by episodic release from intracellular stores. Vasopressin, acting through cAMP, also increases transcription of the aquaporin-2 gene, thus increasing the total number of aquaporin-2 molecules in collecting duct cells.
   Cyclic-AMP activates protein kinase A (PKA) by binding to its regulatory subunits and allowing them to detach from the catalytic subunits. Detachment exposes the catalytic site in the enzyme, allowing it to add phosphate groups to proteins (including the aquaporin-2 protein), which alters their functions.
2. Increasing permeability of the inner medullary portion of the collecting duct to urea by regulating the cell surface expression of urea transporters, which facilitates its reabsorption into the medullary interstitium as it travels down the concentration gradient created by removing water from the connecting tubule, cortical collecting duct, and outer medullary collecting duct.

Cardiovascular system

Vasopressin increases peripheral vascular resistance (vasoconstriction) and thus increases arterial blood pressure. This effect appears small in healthy individuals; however it becomes an important compensatory mechanism for restoring blood pressure in hypovolemic shock such as that which occurs during hemorrhage.

Central nervous system

Avp is expressed in the periventricular region of the hypothalamus in the adult mouse. Allen Brain Atlases

Vasopressin released within the brain has many actions:

• It has been implicated in memory formation, including delayed reflexes, image, short- and long-term memory, though the mechanism remains unknown; these findings are controversial. However, the synthetic vasopressin analogue desmopressin has come to interest as a likely nootropic.

• Vasopressin is released into the brain in a circadian rhythm by neurons of the supraoptic nucleus.

• Vasopressin released from centrally projecting hypothalamic neurons is involved in aggression, blood pressure regulation and temperature regulation.

• It is likely that vasopressin acts in conjunction with corticotropin-releasing hormone to modulate the release of corticosteroids from the adrenal gland in response to stress, particularly during pregnancy and lactation in mammals.

• Selective AVPr1a blockade in the ventral pallidum has been shown to prevent partner preference in prairie voles, suggesting that these receptors in this ventral forebrain region are crucial for pair bonding.

• Recent evidence suggests that vasopressin may have analgesic effects. The analgesia effects of vasopressin were found to be dependent on both stress and gender.

Evidence for this comes from experimental studies in several species, which indicate that the precise distribution of vasopressin and vasopressin receptors in the brain is associated with species-typical patterns of social behavior. In particular, there are consistent differences between monogamous species and promiscuous species in the distribution of AVP receptors, and sometimes in the distribution of vasopressin-containing axons, even when closely related species are compared. Moreover, studies involving either injecting AVP agonists into the brain or blocking the actions of AVP support the hypothesis that vasopressin is involved in aggression toward other males. There is also evidence that differences in the AVP receptor gene between individual members of a species might be predictive of differences in social behavior. One study has suggested that genetic variation in male humans affects pair-bonding behavior. The brain of males uses vasopressin as a reward for forming lasting bonds with a mate, and men with one or two of the genetic alleles are more likely to experience marital discord. The partners of the men with two of the alleles affecting vasopressin reception state disappointing levels of satisfaction, affection, and cohesion. Vasopressin receptors distributed along the reward circuit pathway, to be specific in the ventral pallidum, are activated when AVP is released during social interactions such as mating, in monogamous prairie voles. The activation of the reward circuitry reinforces this behavior, leading to conditioned partner preference, and thereby initiates the formation of a pair bond.

Control

Vasopressin is secreted from the posterior pituitary gland in response to reductions in plasma volume, in response to increases in the plasma osmolality, and in response to cholecystokinin (CCK) secreted by the small intestine:

• Secretion in response to reduced plasma volume is activated by pressure receptors in the veins, atria, and carotids.
• Secretion in response to increases in plasma osmotic pressure is mediated by osmoreceptors in the hypothalamus.
• Secretion in response to increases in plasma CCK is mediated by an unknown pathway.

The neurons that make AVP, in the hypothalamic supraoptic nuclei (SON) and paraventricular nuclei (PVN), are themselves osmoreceptors, but they also receive synaptic input from other osmoreceptors located in regions adjacent to the anterior wall of the third ventricle. These regions include the organum vasculosum of the lamina terminalis and the subfornical organ.

Many factors influence the secretion of vasopressin:

• Ethanol (alcohol) reduces the calcium-dependent secretion of AVP by blocking voltage-gated calcium channels in neurohypophyseal nerve terminals.
• Angiotensin II stimulates AVP secretion, in keeping with its general pressor and pro-volumic effects on the body.
• Atrial natriuretic peptide inhibits AVP secretion, in part by inhibiting Angiotensin II-induced stimulation of AVP secretion.

Secretion

The main stimulus for secretion of vasopressin is increased osmolality of plasma. Reduced volume of extracellular fluid also has this effect, but is a less sensitive mechanism.

The AVP that is measured in peripheral blood is almost all derived from secretion from the posterior pituitary gland (except in cases of AVP-secreting tumours). Vasopressin is produced by magnocellular neurosecretory neurons in the Paraventricular nucleus of hypothalamus (PVN) and Supraoptic nucleus (SON). It then travels down the axon through the infundibulum within neurosecretory granules that are found within Herring bodies, localized swellings of the axons and nerve terminals. These carry the peptide directly to the posterior pituitary gland, where it is stored until released into the blood. However there are two other sources of AVP with important local effects:

• AVP is also synthesized by parvocellular neurosecretory neurons at the PVN, transported and released at the median eminence, which then travels through the hypophyseal portal system to the anterior pituitary where it stimulates corticotropic cells synergistically with CRH to produce ACTH (by itself it is a weak secretagogue).
• Vasopressin is also released into the brain by several different populations of smaller neurons.

Receptors

Below is a table summarizing some of the actions of AVP at its four receptors, differently expressed in different tissues and exerting different actions:

Type	Second messenger system	Locations	Actions
AVPR1A	Phosphatidylinositol/calcium	Liver, kidney, peripheral vasculature, brain	Vasoconstriction, gluconeogenesis, platelet aggregation, and release of factor VIII and von Willebrand factor; social recognition, circadian tau
AVPR1B or AVPR3	Phosphatidylinositol/calcium	Pituitary gland, brain	Adrenocorticotropic hormone secretion in response to stress; social interpretation of olfactory cues
AVPR2	Adenylate cyclase/cAMP	Basolateral membrane of the cells lining the collecting ducts of the kidneys (especially the cortical and outer medullary collecting ducts)	Insertion of aquaporin-2 (AQP2) channels (water channels). This allows water to be reabsorbed down an osmotic gradient, and so the urine is more concentrated. Release of von Willebrand factor and surface expression of P-selectin through exocytosis of Weibel-Palade bodies from endothelial cells
VACM-1	Phosphatidylinositol/calcium	Vascular endothelium and renal collecting tubules	Increases cytosolic calcium and acts as an inverse agonist of cAMP accumulation

Structure and relation to oxytocin

Chemical structure of the argipressin (indicating that this compound is of the vasopressin family with an arginine at the 8th amino acid position.

Chemical structure of oxytocin

The vasopressins are peptides consisting of nine amino acids (nonapeptides). (NB: the value in the table above of 164 amino acids is that obtained before the hormone is activated by cleavage). The amino acid sequence of arginine vasopressin is Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly, with the cysteine residues forming a disulfide bond. Lysine vasopressin has a lysine in place of the arginine.

The structure of oxytocin is very similar to that of the vasopressins: It is also a nonapeptide with a disulfide bridge and its amino acid sequence differs at only two positions (see table below). The two genes are located on the same chromosome separated by a relatively small distance of less than 15,000 bases in most species. The magnocellular neurons that make vasopressin are adjacent to magnocellular neurons that make oxytocin, and are similar in many respects. The similarity of the two peptides can cause some cross-reactions: oxytocin has a slight antidiuretic function, and high levels of AVP can cause uterine contractions.

Below is a table showing the superfamily of vasopressin and oxytocin neuropeptides:

Vertebrate Vasopressin Family
Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2	Argipressin (AVP, ADH)	Most mammals
Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Lys-Gly-NH2	Lypressin (LVP)	Pigs, hippos, warthogs, some marsupials
Cys-Phe-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2	Phenypressin	Some marsupials
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Arg-Gly-NH2	Vasotocin†	Non-mammals
Vertebrate Oxytocin Family
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2	Oxytocin (OXT)	Most mammals, ratfish
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Pro-Gly-NH2	Prol-Oxytocin	Some New World monkeys, northern tree shrews
Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Ile-Gly-NH2	Mesotocin	Most marsupials, all birds, reptiles, amphibians, lungfishes, coelacanths
Cys-Tyr-Ile-Gln-Ser-Cys-Pro-Ile-Gly-NH2	Seritocin	Frogs
Cys-Tyr-Ile-Ser-Asn-Cys-Pro-Ile-Gly-NH2	Isotocin	Bony fishes
Cys-Tyr-Ile-Ser-Asn-Cys-Pro-Gln-Gly-NH2	Glumitocin	Skates
Cys-Tyr-Ile-Asn/Gln-Asn-Cys-Pro-Leu/Val-Gly-NH2	Various tocins	Sharks
Invertebrate VP/OT Superfamily
Cys-Leu-Ile-Thr-Asn-Cys-Pro-Arg-Gly-NH2	Diuretic Hormone	Locust
Cys-Phe-Val-Arg-Asn-Cys-Pro-Thr-Gly-NH2	Annetocin	Earthworm
Cys-Phe-Ile-Arg-Asn-Cys-Pro-Lys-Gly-NH2	Lys-Connopressin	Geography & imperial cone snail, pond snail, sea hare, leech
Cys-Ile-Ile-Arg-Asn-Cys-Pro-Arg-Gly-NH2	Arg-Connopressin	Striped cone snail
Cys-Tyr-Phe-Arg-Asn-Cys-Pro-Ile-Gly-NH2	Cephalotocin	Octopus
Cys-Phe-Trp-Thr-Ser-Cys-Pro-Ile-Gly-NH2	Octopressin	Octopus
†Vasotocin is the evolutionary progenitor of all the vertebrate neurohypophysial hormones.

Role in disease

Lack of AVP

Decreased AVP release or decreased renal sensitivity to AVP leads to diabetes insipidus, a condition featuring hypernatremia (increased blood sodium concentration), polyuria (excess urine production), and polydipsia (thirst).

Excess AVP

High levels of AVP secretion may lead to hyponatremia. In many cases, the AVP secretion is appropriate (due to severe hypovolemia), and the state is labelled "hypovolemic hyponatremia". In certain disease states (heart failure, nephrotic syndrome) the body fluid volume is increased but AVP production is not suppressed for various reasons; this state is labelled "hypervolemic hyponatremia". A proportion of cases of hyponatremia feature neither hyper- nor hypovolemia. In this group (labelled "euvolemic hyponatremia"), AVP secretion is either driven by a lack of cortisol or thyroxine (hypoadrenalism and hypothyroidism, respectively) or a very low level of urinary solute excretion (potomania, low-protein diet), or it is entirely inappropriate. This last category is classified as the syndrome of inappropriate antidiuretic hormone (SIADH).

SIADH in turn can be caused by a number of problems. Some forms of cancer can cause SIADH, particularly small cell lung carcinoma but also a number of other tumors. A variety of diseases affecting the brain or the lung (infections, bleeding) can be the driver behind SIADH. A number of drugs has been associated with SIADH, such as certain antidepressants (serotonin reuptake inhibitors and tricyclic antidepressants), the anticonvulsant carbamazepine, oxytocin (used to induce and stimulate labor), and the chemotherapy drug vincristine. Finally, it can occur without a clear explanation.

Hyponatremia can be treated pharmaceutically through the use of vasopressin receptor antagonists.

Pharmacology

Vasopressin analogues

Vasopressin agonists are used therapeutically in various conditions, and its long-acting synthetic analogue desmopressin is used in conditions featuring low vasopressin secretion, as well as for control of bleeding (in some forms of von Willebrand disease and in mild haemophilia A) and in extreme cases of bedwetting by children. Terlipressin and related analogues are used as vasoconstrictors in certain conditions. Use of vasopressin analogues for esophageal varices commenced in 1970.

Vasopressin infusion has also been used as a second line of management in septic shock patients not responding to high dose of inotropes (e.g., dopamine or norepinephrine).

The role of vasopressin analogues in cardiac arrest

Injection of vasopressors for the treatment of cardiac arrest was first suggested in the literature in 1896 when Austrian scientist Dr. R. Gottlieb described the vasopressor epinephrine as an "infusion of a solution of suprarenal extract [that] would restore circulation when the blood pressure had been lowered to unrecordable levels by chloral hydrate." Modern interest in vasopressors as a treatment for cardiac arrest stem mostly from canine studies performed in the 1960s by anesthesiologists Dr. John W. Pearson and Dr. Joseph Stafford Redding in which they demonstrated improved outcomes with the use of adjunct intracardiac epinephrine injection during resuscitation attempts after induced cardiac arrest. Also contributing to the idea that vasopressors may be useful treatments in cardiac arrest are studies performed in the early to mid 1990's that found significantly higher levels of endogenous serum vasopressin in adults after successful resuscitation from out-of-hospital cardiac arrest compared to those who did not live. Results of animal models have supported the use of either vasopressin or epinephrine in cardiac arrest resuscitation attempts, showing improved coronary perfusion pressure and overall improvement in short-term survival as well as neurological outcomes.

Vasopressin vs. epinephrine

Table 1. Meta-analysis of outcomes for patients treated with vasopressin versus epinephrine

	RR (95% CI)
Failure of ROSC	0.81 (0.58-1.12)
Death before hospital admission	0.72 (0.38-1.39)
Death within 24 hours	0.74 (0.38-1.43)
Death before hospital discharge	0.96 (0.87-1.05)
Number of deaths and neurologically impaired survivors	1.00 (0.94-1.07)

Although both vasopressors, vasopressin and epinephrine differ in that vasopressin does not have direct effects on cardiac contractility as epinephrine does. Thus, vasopressin is theorized to be of increased benefit over epinephrine in cardiac arrest due to its properties of not increasing myocardial and cerebral oxygen demands. This idea has led to the advent of several studies searching for the presence of a clinical difference in benefit of these two treatment choices. Initial small studies demonstrated improved outcomes with vasopressin in comparison to epinephrine. However, subsequent studies have not all been in agreement. Several randomized controlled trials have been unable to reproduce positive results with vasopressin treatment in both return of spontaneous circulation (ROSC) and survival to hospital discharge, including a systematic review and meta-analysis completed in 2005 that found no evidence of a significant difference with vasopressin in five studied outcomes (see Table 1).

Vasopressin and epinephrine vs. epinephrine alone

Table 2. Significant outcomes for combined vasopressin and epinephrine treatment

	RR (95% CI)	p value
ROSC	1.42 (1.14-1.77)
Survival to hospital admission	1.42 (1.02-2.04)	0.05
In subgroup: PEA	1.30 (0.90-2.06)	0.02
In subgroup: Collapse to ED arrival time of 15–30 minutes	1.22 (1.01-1.49)	0.05
In subgroup: Collapse to ED arrival time of 30–45 minutes	1.11 (1.00-1.24)	0.05
Survival to hospital discharge	3.69 (1.52-8.95)

There is no current evidence of significant survival benefit with improved neurological outcomes in patients given combinations of both epinephrine and vasopressin during cardiac arrest. A systematic review from 2008 did, however, find one study that showed a statistically significant improvement in ROSC and survival to hospital discharge with this combination treatment; unfortunately, those patients that survived to hospital discharge had overall poor outcomes and many suffered permanent, severe neurological damage. A more recently published clinical trial out of Singapore has shown similar results, finding combination treatment to only improve the rate of survival to hospital admission, especially in the subgroup analysis of patients with longer "collapse to emergency department" arrival times of 15 to 45 minutes. Table 2 lists all statistically significant findings of a correlation between combined treatment and positive outcomes found in these two studies.

2010 American Heart Association Guidelines

The 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care recommend the consideration of vasopressor treatment in the form of epinephrine in adults with cardiac arrest (Class IIb, LOE A recommendation). Due to the absence of evidence that vasopressin administered instead of or in addition to epinephrine has significant positive outcomes, the guidelines do not currently contain vasopressin as a part of the cardiac arrest algorithms. It does, however, allow for one dose of vasopressin to replace either the first or second dose of epinephrine in the treatment of cardiac arrest (Class IIb, LOE A recommendation).

Vasopressin receptor inhibition

Main article: vasopressin receptor antagonist

A vasopressin receptor antagonist is an agent that interferes with action at the vasopressin receptors. They can be used in the treatment of hyponatremia.

See also

• Oxytocin
• Sexual motivation and hormones
• Vasopressin receptor
• Vasopressin receptor antagonists

References

Further reading

• Rector, Floyd C.; Brenner, Barry M. (2004). Brenner & Rector's the kidney (7th ed.). Philadelphia: Saunders. ISBN 0-7216-0164-2. 

External links

• Molecular neurobiology of social bonding: Implications for autism spectrum disorders a lecture by Prof. Larry Young, Jan. 4, 2010.

English Journal

• Comparison of epinephrine and felypressin pressure effects in 1K1C hypertensive rats treated or not with atenolol.

• Fleury CA1, Andreo VC, Lomba PC, Dionísio TJ, Amaral SL, Santos CF, Faria FA.
• Journal of anesthesia.J Anesth.2015 Feb;29(1):56-64. doi: 10.1007/s00540-014-1866-y. Epub 2014 Jun 25.
• PURPOSE: Epinephrine is considered the gold standard vasoconstrictor for hypertensive patients, but few studies report felypressin's effects. The present study aimed to analyze and compare the effects of these two vasoconstrictors, injected by the intravenous route, on the arterial pressure of normo
• PMID 24962945

• Transient increase in urine protein excretion during treatment with terlipressin and albumin for type-1 hepatorenal syndrome.

• Elia C1, Solà Vergés E2, Rodríguez E1, Ginès P1.
• Journal of hepatology.J Hepatol.2015 Feb;62(2):493-5. doi: 10.1016/j.jhep.2014.09.030. Epub 2014 Oct 2.
• PMID 25283143

• [Response to Terlipressin and albumin is associated with improved outcome in patients with cirrhosis and hepatorenal syndrome].

• Nguyen-Tat M1, Götz E1, Scholz-Kreisel P2, Ahrens J1, Sivanathan V1, Schattenberg J1, Rey JW3, Wörns MA1, Galle PR1, Marquardt JU1.
• Deutsche medizinische Wochenschrift (1946).Dtsch Med Wochenschr.2015 Jan;140(2):e21-6. doi: 10.1055/s-0040-100444. Epub 2015 Jan 22.
• BACKGROUND AND AIM: Hepatorenal syndrome (HRS) is a severe but potentially reversible complication in patients with cirrhosis. Untreated it is associated with a poor prognosis. Several randomized controlled trials (RCT) demonstrated that treatment with terlipressin and albumin improves renal functio
• PMID 25612289

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Also found in: Dictionary/thesaurus, Encyclopedia, Wikipedia, 0.01 sec. lypressin /ly·pres·sin/ (li-pres´in) a synthetic preparation of lysine vasopressin, used as an antidiuretic and vasoconstrictor in the treatment of central diabetes insipidus.

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★リンクテーブル★

リンク元	「リプレッシン」「lysine vasopressin」「リプレシン」

「リプレッシン」

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英

lypressin

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リプレシン、リジンバソプレッシン、リジンバソプレシン

「lysine vasopressin」

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リジンバソプレシン、リジンバソプレッシン

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lypressin

「リプレシン」

　　[★]

英

lypressin

関

リプレッシン