- 1 SIADH: Too much Vasopressin
- 2 Too little Vasopressin
- 3 Clinical Practice
- 4 Vasopressin Overview
- 5 Modus Operandi
- 6 The Benefits of Higher levels of vasopressin
- 7 Its Limitations
- 8 Medical Conditions characterized by Low ADH
- 9 Conditions Associated with High Vasopressin
- 10 How to Increase Vasopressin (AVP Promoters)
- 11 How to Lower Vasopressin (AVP Inhibitors)
Vasopressin, otherwise known as Antidiuretic Hormone (ADH), is produced by the hypothalamus and released by the pituitary gland in the brain. It has roles in water balance and blood pressure, but it’s also sought after as a smart drug. This natural hormone is used in the management of several life-threatening conditions, including bleeding abnormalities and septic shock. Vasopressin is a naturally occurring hormone that helps control various bodily functions. By maintaining the appropriate volume of water in the space that surrounds cells within the body, vasopressin allows proper cellular function.
Vasopressin (also called antidiuretic hormone) plays a role in regulating the circadian rhythm — the periods of sleepiness and wakefulness in a 24-hour cycle. Vasopressin also helps maintain the body’s internal temperature, its blood volume, and the proper flow of urine from the kidneys. Both men and women naturally produce vasopressin, yet men experience its effects more strongly because of how it interacts with the male sex hormone testosterone. Nerve cells at the base of the brain (hypothalamus) make and transport vasopressin to the pituitary gland, which then releases the hormone into the blood stream. Pain, stress, and certain drugs — such as opiates (narcotics) — can trigger the release of vasopressin.
SIADH: Too much Vasopressin
If the body produces too much vasopressin, the kidneys may retain water. This condition is called syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur when the body produces too much or too little vasopressin.
In SIADH, excess water retention dilutes the blood, resulting in a low sodium concentration. Excess vasopressin can be caused by Drug side effects Diseases of the lungs, chest wall, hypothalamus, or pituitary gland Tumors, especially cancerous ones
Too little Vasopressin
Without enough vasopressin, the kidneys may excrete too much water. This causes frequent urination and can lead to dehydration, as well as low blood pressure. Lack of vasopressin can be caused by Damage to the hypothalamus or pituitary glan or Drinking an excessive amount of water
While vasopressin occurs naturally in the body, healthcare providers also use a synthetic vasopressin drug to help manage the following conditions: Diabetes insipidus (a condition in which the kidneys are insensitive to vasopressin because of a tumor, trauma, medication side effect, or inflammation of the pituitary gland or hypothalamus, leading to water loss through frequent urination. Bleeding abnormalities such as von Willebrand disease and mild hemophilia. Esophageal variceal hemorrhage (in which veins in the esophagus become enlarged and bleed) Asystolic cardiac arrest (in which the heart stops beating, with no electrical activity detected) Septic shock (a serious condition involving extremely low blood pressure caused by an infection) For these conditions, vasopressin is given in a hospital or clinical setting, and is administered by injection into a muscle or vein. (1)
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Why is vasopressin so important? Vasopressin plays a major role in keeping your body hydrated, your mind sharp, and your mood bright. If you’re an athlete, you’ll want to make sure your vasopressin isn’t too high, or you will have difficulty holding onto salt, a key electrolyte. If you’re concerned about mental sharpness, you may want to find ways to increase your vasopressin, which is considered a “smart drug” by many and is being studied as a treatment for dementia. If you struggle with frequent urination or if your child struggles with bedwetting, low levels of vasopressin may be to blame. If you feel nauseated after drinking a lot of water or get headaches after intense exercise, your vasopressin may be too high. If you feel like you’re constantly thirsty and always running to the bathroom, your vasopressin is probably on the low side (R). If you do a test and find out your vasopressin is elevated, you may be dealing with stress and/or chronic inflammation (R).
Vasopressin is otherwise known as Arginine-Vasopressin (AVP) because in most species it contains Arginine. It’s also called Antidiuretic Hormone (ADH) because it reduces urination (diuresis). Vasopressin is especially active at night, eliminating the interruption of getting up to go to the bathroom every couple of hours, and allowing you to sleep straight through until morning (R, R2). Besides helping the body to retain water, is also constricts blood vessels, which increases blood pressure. You can think of it as inhibiting flow– of water and of blood. That’s where the name “vasopressin” comes from –causing a restriction in blood vessels.
When the brain gets the signal that the body is getting dehydrated (blood pressure is low, blood is highly concentrated), vasopressin is released and the kidneys are given the message to conserve water and prevent the loss of water in the urine. Instead, the urine is more concentrated and water is reabsorbed into the body, diluting the blood, and restoring balance to the body. Vasopressin does much more than just regulate our water and salt concentrations. It also has a role in memory, regulating blood pressure and body temperature, CRH release, socio-sexual behavior, and even our circadian rhythm (R). It can act as a neurotransmitter, and it can stimulate the production of other needed neurotransmitters (R). Vasopressin is also considered to be a stress hormone like cortisol or CRH (R).
The Benefits of Higher levels of vasopressin
Vasopressin is used as a nootropic/smart drug. Vasopressin increases mental clarity, attention to detail, short-term memory (R, R2) and long-term memory (R, R2). It enhances learning in mice (R). It is also being considered for the treatment of memory problems associated with aging, dementia, drug toxicity, and amnesia. (R) High Vasopressin can make you more cooperative (R).
Medical Conditions characterized by Low ADH
Bed wetting (R). Diabetes Insipidus (R). Chronic Inflammatory Response Syndrome (based on anecdotes from Shoemaker, which may not be true, since the testing used isn’t accurate). Most healthy patients have vasopressin come in at under 1. Insomnia in the elderly – vasopressin nose sprays increase sleep quality in older subjects (R, R2). Slow gut flow (motility) in the digestive tract (in rabbits) (R). Vasopressin has also been found in the human digestive tract with implications for involvement there (R).
Conditions Associated with High Vasopressin
Stress -in humans (R, R2) and in rats (R) and mice (R). Pain – in humans (R). High blood pressure (R). Major depression (R). Diabetes (Type 2) (R). Low Cortisol (R). Low sodium/Hyponatremia/ Syndrome of Inappropriate Diuretic Hormone (SIADH) secretion Unsteady gait (R) impaired memory (R) Low Thyroid (R). Post Viral Fatigue Syndrome (R). Autism (R). Kidney Stones – Vasopressin causes our urine to be less dilute (R). High Blood Sugar – Insulin can cause the release of vasopressin (R). Vasopressin causes insulin release in mice (R). Low BUN (Blood Urea Nitrogen) levels (R). Low Uric Acid levels particularly in SIADH (R). High CRH – Vasopressin releases CRH (R). Anorexia – vasopressin suppresses appetite (R, R2).
How to Increase Vasopressin (AVP Promoters)
Restricting water (R). Dietary Sodium (R). Standing (R). Exercise (R). Sauna (R)Forskolin/cAMP (R)Glycine (R, R2) Rhodiola – Lowers endopeptidase activity, leading to higher vasopressin. Rhodiola sacra (R) and Rhodiola sachalinensis (R). I couldn’t find a study using the more common, Rhodiola rosea. Ginkgo – Lowers endopeptidase activity, leading to higher vasopressin (R) Baicalein – Inhibits endopeptidase, raising vasopressin (R). Berberine – Inhibits endopeptidase, raising vasopressin (R). acetylcholine – Increases vasopressin (in rat studies) (R, R2). Increase IL-1beta (R).Increase Interleukin-6 (R). Increase CRH, which increases vasopressin (R). Inhibit IGF-1, which inhibits vasopressin (R). Increase BMAL1, which is needed for the production of vasopressin (R). Ways to increase BMAL1 include DHA (R), increasing SIRT1 (R), and increasing AMPK (works by decreasing CRY1) (R). Stimulate 5-HT2C receptors, which leads to an increase in vasopressin (R). Some 5-HT2C activators include Serotonin (R), Ginseng (R), and Bacopa (rats) (R).
Vasopressin – Vasopressin is also used as a nootropic/smart drug. Ask your doctor about vasopressin. Nicotine (rabbits, cats, men ) (R1, R2, R3). Racetams – Raise Acetylcholine, raising vasopressin Pramiracetam – Inhibits endopeptidase, raising vasopressin (R)..
How to Lower Vasopressin (AVP Inhibitors)
- Lithium – In human studies (R).
- Decrease Interleukin-6 (R).
- Decrease IL-1beta (R).
- Decrease CRH – CRH increases Vasopressin (R).
- Increase MSH – MSH decreases ADH/Vasopressin in rat studies (R).
- Increase IGF-1, which inhibits vasopressin (R).
- Increase Progesterone – Progesterone therapy caused a decrease in blood levels of vasopressin (R).
- Combine Estrogen with Progesterone – There was no change in blood levels of vasopressin with estrogen treatment alone, but following a combined administration of estrogen and progesterone (R).
- Increase Testosterone (R).
- Increase Oxytocin – under certain circumstances, oxytocin indirectly inhibits the release of stress hormones such as cortisol and, in those situations, may be considered an antagonist of vasopressin (R).
- Alcohol – Inhibits vasopressin (R).
- Decrease BMAL1, which is needed for the production of vasopressin (R).
A third function is possible. Some AVP may be released directly into the brain from the hypothalamus, and may play an important role in social behavior, sexual motivation and pair bonding, and maternal responses to stress.
Vasopressin induces differential of stem cells into cardiomyocytes and promotes heart muscle homeostasis.
It has a very short half-life, between 16–24 minutes.
Vasopressin regulates the tonicity of body fluids. It is released from the posterior pituitary in response to hypertonicity and causes the kidneys to reabsorb solute-free water and return it to the circulation from the tubules of the nephron, thus returning the tonicity of the body fluids toward normal. An incidental consequence of this renal reabsorption of water is concentrated urine and reduced urine volume. AVP released in high concentrations may also raise blood pressure by inducing moderate vasoconstriction.
AVP also may have a variety of neurological effects on the brain. It may 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.
Vasopressin has three main effects:
- Increasing the water permeability of initial and cortical collecting tubules (ICT & CCT), as well as outer and inner medullary collecting duct (OMCD & IMCD) in the kidney, thus allowing water reabsorption and excretion of more concentrated urine, i.e., antidiuresis. This occurs through increased transcription and insertion of water channels (Aquaporin-2) into the apical membrane of collecting 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. This effect is mediated by V2 receptors. 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.
- 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 interstitiumas it travels down the concentration gradient created by removing water from the connecting tubule, cortical collecting duct, and outer medullary collecting duct.
- Acute increase of sodium absorption across the ascending loop of henle. This adds to the countercurrent multiplication which aids in proper water reabsorption later in the distal tubule and collecting duct.
Vasopressin released within the brain may have several actions:
- Vasopressin is released into the brain in a circadian rhythm by neurons of the suprachiasmatic nucleus.
- Vasopressin released from centrally projecting hypothalamic neurons is involved in aggression, blood pressure regulation, and temperature regulation.–>
- Recent evidence suggests that vasopressin may have analgesic effects. The analgesia effects of vasopressin were found to be dependent on both stress and sex.
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 in rats.
- 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.
- Cortisol inhibits secretion of antidiuretic hormone.
The physiologic stimulus for secretion of vasopressin is increased osmolality of the plasma, monitored by the hypothalamus. A decreased arterial blood volume, (such as can occur in cirrhosis, nephrosis and heart failure), stimulates secretion, even in the face of decreased osmolality of the plasma: it supersedes osmolality, but with a milder effect. In other words, vasopressin is secreted in spite of the presence of hypoosmolality (hyponatremia) when the arterial blood volume is low.
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.
There are other sources of AVP, beyond the hypothalamic magnocellular neurons. For example, AVP is also synthesized by parvocellular neurosecretory neurons of the PVN, transported and released at the median eminence, from which it 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).
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 (argipressin) is Cys–Tyr–Phe–Gln–Asn–Cys–Pro–Arg–Gly-NH2, with the cysteine residues forming a disulfide bond and the C-terminus of the sequence converted to a primary amide.Lysine vasopressin (lypressin) has a lysine in place of the arginine as the eighth amino acid, and is found in pigs and some related animals, whereas arginine vasopressin is found in humans.
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 secrete vasopressin are adjacent to magnocellular neurons that secrete 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:
Vasopressin is used to manage anti-diuretic hormone deficiency. It has off-label uses and is used in the treatment of vasodilatory shock, gastrointestinal bleeding, ventricular tachycardia and ventricular fibrillation. Vasopressin is used to treat diabetes insipidus related to low levels of antiduretic hormone. It is available as Pressyn.
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 infusions are also used as second line therapy for septic shock patients not responding to fluid resuscitation or infusions of catecholamines (e.g., dopamineor norepinephrine) to increase the blood pressure while sparing the use of catecholamines. These argipressins have much shorter elimination half-life (around 20 minutes) comparing to synthetic non-arginine vasopresines with much longer elimination half-life of many hours. Further, argipressins act on V1a, V1b, and V2 reseptors which consequently lead to higher eGFR and lower vascular resistance in the lungs. A number of injectable arginine vasopressins are currently in clinical use in the United States and in Europe.
Vasopressin is administered through an intravenous device, intramuscular injection or a subcutaneous injection. The duration of action depends on the mode of administration and ranges from thirty minutes to two hours. It has a half life of ten to twenty minutes. It is widely distributed throughout the body and remains in the extracellular fluid. It is degraded by the liver and excreted through the kidneys.. Arginin vasopressins for use in septic shock are intended for intravenouse use only.
The most common side effects during treatment with vasopressin are dizziness, angina, chest pain, abdominal cramps, heartburn, nausea, vomiting, trembling, fever, water intoxication, pounding sensation in the head, diarrhea, sweating, paleness, and flatulence. The most severe adverse reactions are myocardial infarction and hypersensitivy.
The use of lysine vasopressin is contraindicated in the presence of hypersentivity to beef or pork proteins, increased BUN and chronic renal failure. It recommended that it be cautiously used in instances of perioperative polyuria, sensitivity to the drug, asthma, seizures, heart failure, a comatose state, migraine headaches, and cardiovascular disease.
- alcohol – may lower the antidiuretic effect
- carbamazepine, chloropropamide, clofibrate, tricyclic antidepressants fludrocortisone may raise the diuretic effect
- lithium, demeclocycline, heparin or norepinephrine may lower the antidiuretic effect
- vasopressor effect may be higher with the concurrent use of ganglionic blocking medications
There may be a connection between arginine vasopressin and autism.
Decreased AVP release (neurogenic — i.e. due to alcohol intoxication or tumour) or decreased renal sensitivity to AVP (nephrogenic, i.e. by mutation of V2 receptor or AQP) leads to diabetes insipidus, a condition featuring hypernatremia (increased blood sodium concentration), polyuria (excess urine production), and polydipsia (thirst).
Syndrome of Inappropriate Antidiuretic Hormone secretion (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. It has also been associated with fluoroquinolones (including ciprofloxacin and moxifloxacin). Finally, it can occur without a clear explanation. Hyponatremia can be treated pharmaceutically through the use of vasopressin receptor antagonists.
Vasopressin was elucidated and synthesized for the first time by Vincent du Vigneaud.
Evidence for an effect of AVP on monogamy vs promiscuity 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.
- Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH)
- Sexual motivation and hormones
- Vasopressin receptor
- Vasopressin receptor antagonists
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