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From Wikipedia, the free encyclopedia

Vasotocin
Names
IUPAC name
1-[(1R,4S,7S,13S,16R)-16-amino-4-(2-amino-2-oxoethyl)-7-(3-amino-3-oxopropyl)-10-[(2S)-butan-2-yl]-13-[(4-hydroxyphenyl)methyl]-3,6,9,12,15-pentaoxo-18,19-dithia-2,5,8,11,14-pentazacycloicosane-1-carbonyl]-N-[(2S)-1-[(2-amino-2-oxoethyl)amino]-5-(diaminomethylideneamino)-1-oxopentan-2-yl]pyrrolidine-2-carboxamide
Other names
Argiprestocin; Arg-vasotocin; 8-Arg-vasotocin; Arginine vasotocin
Identifiers
3D model (JSmol)
ChEBI
ECHA InfoCard 100.245.670 Edit this at Wikidata
UNII
  • NC(=O)CNC(=O)[C@H](CCCN=C(N)N)NC(=O)C1CCCN1C(=O)[C@H]2NC(=O)[C@H](CC(=O)N)NC(=O)[C@H](CCC(=O)N)NC(=O)[C@H]([C@H](CC)C)NC(=O)[C@H](Cc3ccc(O)cc3)NC(=O)[C@@H](N)CSSC2
Properties
C43H67N15O12S2
Molar mass 1050.22 g·mol−1
Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
☒N verify (what is checkY☒N ?)

Vasotocin is an oligopeptide homologous to oxytocin and vasopressin found in all non-mammalian vertebrates (including birds, fishes, and amphibians) and possibly in mammals during the fetal stage of development. Arginine vasotocin (AVT), a hormone produced by neurosecretory cells within the posterior pituitary gland (neurohypophysis) of the brain, is a major endocrine regulator of water balance and osmotic homoeostasis and is involved in social and sexual behavior in non-mammalian vertebrates. In mammals, it appears to have biological properties similar to those of oxytocin (stimulating reproductive tract contraction as in egg laying or birth) and vasopressin (diuretic and antidiuretic effects). It has been found to have effects on the regulation of REM sleep.[1] Evidence for the existence of endogenous vasotocin in mammals is limited[2][3] and no mammalian gene encoding vasotocin has been confirmed.

AVT (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Arg-Gly-NH2), which occurs in the lamprey, represents the ancestral form in the phylogeny of the vertebrate neurohypophysial hormones.[4] Gene duplication and point mutation have produced two distinct lineages, one involved in reproduction (oxytocin-like peptides) and the other in osmoregulation (vasopressin-like peptides). These hormones have remained highly conserved throughout evolution. Each is a peptide of nine amino acids derived from a preprohormone precursor by proteolytic cleavage, with an intramolecular disulfide bridge between the cysteine (Cys) residues; the C-terminal glycine (Gly) residue is amidated. Six of the residues have been found to be invariant in homologous peptides from numerous species of vertebrates. The vasopressin-like peptides, which differ in positions 3 and/or 8, include AVT and the mammalian hormones arginine vasopressin (Cys-Tyr-Phe-Gln-Asn-Cys-Pro-Arg-Gly-NH2, with isoleucine-3 of AVT changed to phenylalanine) and lysine vasopressin (isoleucine-3 changed to phenylalanine and arginine-8 changed to lysine). The oxytocin-like peptides, which differ in positions 4 and/or 8, include oxytocin (Cys-Tyr-Ile-Gln-Asn-Cys-Pro-Leu-Gly-NH2, with arginine-8 of AVT changed to leucine), mesotocin (arginine-8 changed to isoleucine), and isotocin (glutamine-4 changed to serine and arginine-8 changed to isoleucine); they differ from the vasopressin-like peptides in having a neutral amino acid in place of a basic amino acid at position 8. Oxytocin occurs in placental mammals; mesotocin occurs in amphibians, reptiles, and birds, and isotocin occurs in fishes.

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Transcription

We're going to talk about antidiuretic hormone. And you can see I've already started drawing for this video. And the main reason is because I'm not a great drawer, and I wanted to make sure that everything was pretty clear. And so I drew out on one side the pituitary gland and on the other the brain. And so antidiuretic hormone-- I underlined ADH because that's usually what it's called. People call it ADH. Sometimes people call it vasopressin as well. Actually, vasopressin is good because it's useful. You can see "vaso" kind of refers to blood vessels, and "pressin" kind of squeezing down on blood vessels. It gives you a clue as to what the hormone is doing. So I've drawn for you the hypothalamus here. Also, right below it, this would be kind of the infundibulum, kind of the neck. And at the very bottom, the pituitary. So this is the actual pituitary down here. And there's a front and back to this. And the front, facing forward closer to the eyes, would be the anterior pituitary. So that'd be over here. And back here, this lobe would be the posterior pituitary because it's a little bit further back. And since we're naming stuff, let me just go ahead and round it out. This right here is actually the optic chiasm. It has to do with vision. So I'm just going to write optic chiasm so you know what we're talking about. And the only reason I even bring that up is because just above it-- let's say in this area-- just above it. And if I was to draw it over on my little diagram-- that'd be maybe right there-- is what's called the "supra"-- S-U-P-R-A-- supraoptic nucleus. And nucleus here just refers to a collection of nerve cell bodies, not the nucleus we usually think of-- meaning not the one where it's sitting inside of a cell and kind of directing the flow of traffic in the brains of the cell in a way of saying it. But here the nucleus is actually just a collection of little nerve cell bodies. And I'm actually just going to draw two, but you know there's actually many more there. This is just for diagram purposes. And actually, if I was to draw the rest of this nerve, you would actually go all the way down. And this is actually beginning to share with you some of the cool aspects of this hypothalamus and the posterior pituitary. You can see that, basically, these nerve cells start in one spot, and they go all the way down to the posterior pituitary through that infundibulum. This is how the hypothalamus and posterior pituitary are connected-- through nerves. And these nerves are actually full of the hormone ADH. So we've already talked about the fact that this is related to ADH, but now you can see exactly how. ADH is actually being made in these nerve cells. And it's actually sitting here waiting for the right moment for these nerves to release it. And this ADH is actually a small protein. It's nine amino acids long. So it's actually pretty small. This is ADH. Nine amino acids. So it's pretty teeny, and it's a hormone. And if you know it's an amino acid-based hormone, you can think of it as a peptide or a protein hormone and distinguish it from the steroid hormones. So this is how ADH is made. It's made in these nerve cells. And the next thing to talk about is how it's released. And so if you have, let's say, a little capillary bed in here with little arterials and capillaries coming together into little venules on this side, what happens is that, when there's a trigger-- and actually, maybe I should write that in a very bold color. Let's say red. That's my favorite bold color. When there's a trigger, these nerve cells right here are going to fire off their ADH. They're going to release all that ADH, and it's going to dump right here into this area where all the capillaries are. And of course, the flow of blood is going to carry all that ADH into the little vein-- and let me draw the venule and the vein-- and basically, take it to the rest of the body. So this is how ADH actually gets released out of the nerve cells that live in the supraoptic nucleus and gets out to the body. It basically does it by dumping into that posterior pituitary and getting picked up by all those little capillaries and venules. So I guess the next issue is to figure out what is the trigger? So what is the trigger for this little supraoptic nucleus that I've drawn here? So let's talk about that. Let me make some space. There. Now, we've got a clean bit of canvas. So let's talk about the triggers that our body uses to know when to fire off that ADH to get it released. The main trigger-- and this is probably the one trigger that you want to take away. If you're going to forget everything else, try to remember this one. The main trigger is going to be high blood concentration. And the way we think about blood concentration is in osmolarity. Let me write that down. What osmolarity refers to is, if you took all the solutes that are floating around in the blood-- so that includes everything from protein to sodium to potassium, everything that is going to drag water into the blood vessels-- if you combine all that, then what is your total blood concentration going to be? And you can almost think of it as a meter. So let me draw it for you. Like a little meter here. On one side, you've got-- let's say something like that. And on one side, let's say you've got 260, and on the other side 320. And this is just concentrations. So 280 and 300. And this is osms per liter. And actually, these are the units here. So osmolarity as measured in osms per liter. So this is the concentration. And what you want to do is you want to really stay in this area right here. This is kind of your green zone. This is where the body likes to be, generally speaking. And if it's here, if it's in this area, or if it's in this area, then that's where the body is not too happy. And so for example, let's say you're in this first zone. This would mean that your body is noticing that the blood is too dilute. And if it's on this side, your body's noticing that it's too salty. The body is saying that the blood is too salty. And so in this case, if you have, let's say-- like I said-- a meter down here, if the needle is falling in this area, then that's going to be a trigger for ADH release. So that's the first trigger that we can talk about. In fact, why don't I even go back up and add that to our diagram? So I'm going to put that into our diagram so that we can see it very clearly as being one of the triggers. So let's imagine you have right here a little nerve cell. And I'm going to draw it this way purposefully because we actually don't know where these little osmoreceptors are. All we know is that they do a fantastic job, but we don't know exactly where these osmoreceptors are. And this is my little diagram that I drew before. And you can now think, if the osmoreceptor is telling you that it's over there, then that's a problem. And in fact, why I don't I even go one step further and label this as my osmoreceptor? So if my osmoreceptor is set to tell me that it's too salty, that is one of the signals that's going to trigger ADH release. OK. So now, what's the second trigger? What's another reason why we might release ADH? Low blood volume. Think about that for a second. How in the world would your body even know that the blood volume is too low? Well, let's go back to basics. Let's go back to the heart. That's where I like to begin because that's how I always think about it. Just very simply, what is going into the heart, and what's coming out? Well, we know we have blood vessels-- large ones, in fact, large veins-- dumping into the heart. So we have the superior and inferior vena cava. This is the superior vena cava-- this is a large vein-- and this is the inferior vena cava. These aren't the only large veins, but these are two examples of large veins. And we also have the right atrium. So we have a couple of spots here that are in the blood vessels where we might have little nerve endings. So nerve endings in these areas are going to start recognizing when the blood volume is low. Because, remember, the venous system-- this is kind of a stretch-- the venous stretch from something we talked about a long time ago. The venous system is actually going to be a large volume system. So if there's ever a decrease in the volume, that would be one of the best places to figure it out. So information in the walls-- so basically, these nerve fibers, rather, in the walls of the vessels are going to be less stretched. And they're going to say, well, why are we less stretched? And the answer is that there's actually less blood volume. So when they're less stretched, they're going to send a signal and say, hey, something's up. We have less blood volume, and I think the brain needs to know about that. So that's how a signal gets sent all the way up to the brain. And actually, I can draw that in as well. So let's put in a little receptor here. And now, these are going to go down and sense low volume from those receptors in the large veins and the right atrium. OK. Now, what's another trigger? You can see there are a lot of different triggers. I'm putting up one after another. Let's put another trigger up there. What's another reason why ADH would be secreted? Well, maybe a decrease in blood pressure. Now, we know that the veins tell us a lot of information about volume. So it might extend that the arteries can tell us about pressure. And you might recall from another video where we talked about baroreceptors that this is a fantastic way to get information about pressure. So let me draw some of those baroreceptors. And baroreceptor just refers to pressure receptor. We have baroreceptors that are in the aortic arch right there. And we also have baroreceptors that are in the carotid sinuses on both sides. So these baroreceptors are going to recognize when the blood pressure is starting to go low. And they're going to send a signal up to the brain to say, hey, again, we need to do something about this. Our pressure is low. So that's another signal up to the brain. And that we can draw it right here. We could say, OK. Maybe something like this. And that would be a signal about low-- let's write that here-- low pressure. So now we've got signals about high osmolarity, low volume, low pressure. Are there any other signals that we can think of? One more jumps to my mind-- angiotensin 2. Remember, angiotensin 2 is actually part of the whole RAS system-- the renin-angiotensin-- or I'll just write AT-- aldosterone system. And so angiotensin 2 is actually going to be another trigger. So you can actually imagine through a blood vessel, and you might have a nerve nearby. And this is going to trigger right here this molecule of angiotensin, which has eight little amino acids. It's going to be a signal to that nerve that it needs to let the body know-- or the brain know, rather, that pressures are low. This is another signal. And let me just write that up here in our picture. Another signal could be something like this. Maybe right here. And the exact location that I'm drawing is actually just kind of arbitrary, but the idea is that you have angiotensin 2 having effects on the brain as well. So this little molecule is going to come and let the brain know that, hey, even the kidneys are trying to do something about the blood pressure. And it would be great if the brain got involved in releasing some ADH, if needed. So these are the different triggers. And like I said in the beginning, probably the main one you want to think about-- as far as ADH is concerned-- is this osmoreceptor. This is really the most important one because everything else is secondary to that. That is definitely the major function of ADH.

Biosynthesis

AVT is synthesized as a preprohormone that includes a second peptide, neurophysin VT (neurophysins are carrier proteins that are secreted along with their passenger hormones); intracellular proteolytic processing generates the mature peptides. In the chicken (Gallus gallus), the 161-amino acid vasotocin-neurophysin VT preprohormone is encoded by the gene AVP, which is considered homologous to the mammalian genes encoding arginine vasopressin.[5] Removal of the 19-amino acid N-terminal signal peptide generates the prohormone, which is hydrolysed to AVT (derived from amino acids 20-28) and neurophysin VT (derived from amino acids 32-161).[6] The existence of two AVT preprohormones with different sequences in fishes (such as chum salmon, Oncorhynchus keta[7]) is evidence for gene duplication.

Physiological effects

AVT combines both antidiuretic and reproductive activities similar to those of oxytocin and vasopressin. The physiological actions of AVT in birds are mediated through diverse receptor subtypes VT1, VT2, VT3 and VT4.[8] AVT and synthetic analogs injected into monkeys cause reabsorption of osmotically free water and changes in excretion of sodium and potassium ions in the kidneys.[9] AVT produces distinct effects on the reproductive functions of male and female domestic chickens. In laying hens, AVT synthesised in magnocellular diencephalic neurons is released into circulation in a highly coordinated manner, contributing to the peripheral control of oviposition. In males, parvocellular AVT cells located in the limbic system (bed nucleus of stria terminalis) express AVT. This expression is sensitive to gonadal steroids and is correlated with sexual differentiation of masculine behavior such as courtship vocalization and copulation.[8]

Behavioral effects

Several animal studies have been conducted that explore the behavioral effects of AVT. The main findings of these studies have revealed that AVT plays an integral role in the pair bonding behavior and social hierarchy in non-mammalian vertebrates.

In a study conducted with zebra finches,[10] increased levels of AVT were linked to an increase in aggressive, competitive behavior in non-paired male finches, but were subsequently related to an increase in defensive behavior after the finches had been paired. However, this study also found that blocking AVT receptors did not directly affect pair bonding ability. The shift in behaviors were explained by the location of the release of AVT in the brain. Competitive aggressive behavior was found to be linked with AVT release in the BSTm, whereas defensive, nest-protecting behavior was linked with AVT release in the neurons of the Hypothalamus and Paraventricular Nucleus.

In a study conducted with male Japanese quail, AVT was found to have an effect on later social interactions amongst the species. Immediately after injection with AVT, the quails displayed less aggressive behavior (pecking). However, the next day, the quail that were injected with AVT displayed more dominant behavior towards familiar birds, but not unfamiliar birds. This study shows that AVT may play a role in establishing social hierarchy.[11]

A study that investigated the role of social construction and AVT compared territorial and non-territorial species of tropical coral reef fish.[12] Experimenters administered Manning compound, an AVT agonist to the fish and found that, after treatment, non-territorial species displayed more territorial behavior whereas territorial species displayed less territorial behavior.

Research suggests that the effects of AVT on aggression may be influenced by the social construction of the species. For example, in a study done with Rainbow Trout,[13] increased levels of AVT were associated with more subordinate behavior. It is currently hypothesized that the contrasting effects of AVT are related to the distinction between territorial versus colonial social systems. In a territorial species, such as Rainbow Trout, AVT is linked to less dominant behavior. This may be due to the differences in the distribution of AVT receptors in territorial and colonial species.

Sources

  1. ^ Kales, Anthony (1995). The Pharmacology of sleep. Berlin: Springer-Verlag. ISBN 3-540-58961-9.
  2. ^ Ervin MG, Leake RD, Ross MG, Calvario GC, Fisher DA (May 1985). "Arginine vasotocin in ovine fetal blood, urine, and amniotic fluid". J Clin Invest. 75 (5): 1696–701. doi:10.1172/JCI111878. PMC 425513. PMID 3998151.
  3. ^ Ervin MG, Amico JA, Leake RD, Ross MG, Robinson AG, Fisher DA (1988). "Arginine vasotocin and a novel oxytocin-vasotocin-like material in plasma of human newborns". Biol Neonate. 53 (1): 17–22. doi:10.1159/000242757. PMID 3355867.
  4. ^ Liu JW, Ben-Jonathan N (January 1994). "Prolactin-releasing activity of neurohypophysial hormones: structure-function relationship". Endocrinology. 134 (1): 114–18. doi:10.1210/endo.134.1.8275925. PMID 8275925.
  5. ^ "AVP arginine vasopressin (neurophysin II, antidiuretic hormone, diabetes insipidus, neurohypophyseal) [ Gallus gallus (chicken) ], Entrez Gene ID 396101".
  6. ^ "Vasotocin-neurophysin VT, UniProtKB/Swiss-Prot P24787 (NEUV_CHICK)".
  7. ^ Heierhorst J, Mahlmann S, Morley SD, Coe IR, Sherwood NM, Richter D (January 1990). "Molecular cloning of two distinct vasotocin precursor cDNAs from chum salmon (Oncorhynchus keta) suggests an ancient gene duplication". FEBS Lett. 260 (2): 301–4. doi:10.1016/0014-5793(90)80129-7. PMID 2298304. S2CID 24247029.
  8. ^ a b Jurkevich A, Grossmann R (2003). Vasotocin and reproductive functions of the domestic chicken. Domest Anim Endocrinol. 25(1):93-9. PMID 12963102
  9. ^ Buravkova LB, Larina IM, Korolkov VI, Dobrokhotov IV, Grigorev AI (2003). Bull Exp Biol Med. 142(6):714-6. PMID 17603678
  10. ^ Kabelik D, Klatt JD, Kingsbury MA, Goodson JL. Endogenous vasotocin exerts contexts-dependent behavioral effects in semi-naturalistic colony environment. Hormones and Behavior. 2009;56(1): 101-107.
  11. ^ Riters LV, and Panksepp J. Effects of vasotocin on aggressive behavior in male Japanese quail. Annals of the New York Academy of Sciences. 2006; 807(1): 478-480.
  12. ^ Semsar K, Kandel FLM, Godwin J. Manipulations of the AVT system shift social status and related courtship behavior in the Bluehead Wrasse. Hormones and Behavior. 2001; 40(1): 21-31.
  13. ^ Backström T, and Winberg S. Arginine vasotocin influence on aggressive behavior and dominance in rainbow trout. Physiology and Behavior. 2009; 96(3): 470-475.

External links

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