Talk:Vasopressin
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[edit] Move
I feel like this article should be moved to Vasopressin. First of all, it would allow us to quickly get out of the way the issue of arginine vasopressin vs. lysine vasopressin. More importantly, the actions of vasopressin go way beyond water retention, etc.. ADH is a pretty outdated name. AVP has a lot of important neuralpeptide actions, as a social recognition signal in the forebrain. Hard to get into this in the current article structure and with the current title. --Chinasaur 19:14, 28 Jan 2005 (UTC)
- Vasopressin is probably a good title, and is increasingly being used instead of ADH. It is, incidentally, still not indicative of its function outside the vascular and renal signal transduction systems. Could you please add more about the social recognition signal role? I know nothing about this! JFW | T@lk 02:12, 30 Jan 2005 (UTC)
Just a note from a google searcher... Both articles (ADH and Vasopressin) are practically the same, and neither mentions VP's effect on urea reabsorption, which is a fairly important effect.
- The articles are identical: vasopressin redirects here. Why is urea reabsorption so important in this article? JFW | T@lk 15:39, 25 January 2006 (UTC)
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- ADH's effect on urine concentration isn't only due to its effects on water permeability; a large part of this effect is from ADH's contribution to the osmolality of the medullary interstitium, which is where urea is of great importance. ADH acts on the inner medullary collecting tubules, raising their permeability to urea and allowing its reabsorption. This raises the interstitial osmolality substantially (by as much as 500-600 mOsm/kg), which — combined with the increased collecting duct water permeability — drives the reabsorption of water from the collecting duct, leading to highly concentrated urine. --David Iberri (talk) 03:47, 15 March 2006 (UTC)
[edit] Official name of vasopressin
I was recently taught that ADH is the better name, and that vasopressin is outdated - higher quantities are needed for ADH to act as vasopressin, and its primary function is as an anti-diuretic hormone - ie, it stops diuresis. Also, there is still no mention of urea in the article - I don't feel qualified to put this in, but it does seem like rather a large omission. 131.111.8.104 11:19, 16 May 2007 (UTC)
- AVP is the official name agreed upon by the international naming association. Also, probably very few named substances are limited to what their name implies. AVP, for example, has many roles in the brain regulating various behaviors that are important for understanding human social interactions. AlbertHall 13:58, 16 May 2007 (UTC)
- The approved gene symbol and name is arginine vasopressin (see [1]).
[edit] Misc.
There is an error in the second infobox, but I haven't a clue how to fix those prot box things. Fuzzform 20:08, 11 February 2006 (UTC)
- What's the error? AxelBoldt 01:49, 12 February 2006 (UTC)
Some references to all the various effects of vasopressin would be nice...
- Vasopressin is secreted from parvocellular neurons
Should "parvocellular" be linked to parvocellular part or is this a different use of the term? AxelBoldt 15:27, 6 April 2006 (UTC)
-
- The terms refer to different things. That article refers to part of the lateral geniculate nucleus, which is involved in the visual system. In the context of AVP, parvocellular refers to cells of the paraventricular nucleus. So no linkage necessary. --David Iberri (talk) 18:03, 6 April 2006 (UTC)
DDAVP induced VWF release goes through the vasopressin-2 receptor. This is a cAMP-mediated process. Prayingmantis78 18:58, 4 June 2007 (UTC)
[edit] Dosages for asystolic arrest?
I would like to see the vasopressin dosages typically used in asystolic arrest posted. 75.19.187.142 18:40, 1 April 2007 (UTC)Yaek
- The 2005 AHA guidelines note one 40 U dose of vasopressin may be used in lieu of epinephrine in "all pulseless cardiac arrest scenarios", including asystole. On a side note, WP:MEDMOS discourages the addition of dosing information to articles. Fvasconcellos 18:50, 1 April 2007 (UTC)
[edit] caffeine and vasopressin- Reference?
Caffeine is certainly a diuretic and natriuretic, but I can't find any original research article saying caffeine decreases vasopressin release. I found one saying it may be having its effect via adenosine receptors. Timo Rieg, Hannah Steigele, Jurgen Schnermann, Kerstin Richter, Hartmut Osswald, and Volker Vallon. Requirement of intact adenosine A1 receptors for the diuretic and natriuretic action of the methylxanthines theophylline and caffeine. J Pharmacol Exp Ther. 2005 Apr;313(1):403-9. Epub 2004 Dec 8. Misskidney 19:49, 16 April 2007 (UTC)
- I was just here to say the same thing. Indeed the diuretic article lists caffiene as a sodium reabsorption inhibitor and not as a vasopressin inhibitor. Potkettle 12:05, 30 July 2007 (UTC)
[edit] ADH is definitely a more appropriate name
The name vasopressin is indeed outdated, all newer textbooks I've seen use ADH. Vasoconstriction is only a tertiary fuction of this hormone expressed in the extreme case of hemorrage. Its main function is homeostasis as antidiuretic hormone therefore ADH is definitely a more appropriate name. EerieNight 11:02, 25 August 2007 (UTC)
- You may believe that vasopressin is outdated, but that train has left the station. The international nomenclature commission has assigned vasopressn and AVP as the official name and symbol, respectively, for the gene and peptide. And, although ADH describes its action at the kidney, it fails as much as AVP does to describe the equally important actions of vasopressin at the pituitary and within the brain.AlbertHall 16:52, 25 August 2007 (UTC)
[edit] WikiProject class rating
This article was automatically assessed because at least one WikiProject had rated the article as start, and the rating on other projects was brought up to start class. BetacommandBot 16:32, 10 November 2007 (UTC)
[edit] Aren't there higher levels of vasopressin in males than in females?
Anyone know why this is? 72.161.203.107 (talk) 02:15, 19 November 2007 (UTC)
- That is true in a few brain areas but if you are talking about total vasopressin in the animal, that contribution is miniscule. AlbertHall (talk) 13:28, 19 November 2007 (UTC)
[edit] In need of Revision
Under the Kidney Action section. I think the discussion of the G protein-coupled receptor, and cAMP second messenger systems are inappropriate. A description of the V2 receptor as a G protein-coupled receptor acting by a cAMP second messenger system would be a sufficient description. For the interim I have left the section unchanged except for a link to the appropriate article. —Preceding unsigned comment added by Backwardtoes (talk • contribs) 10:14, 15 December 2007 (UTC)
[edit] This article should be revised
The description of G protein signaling by G alpha s within the "Kidney" chapter is a crap.
G protein alpha subunit does exchange GDP by GTP for activation and not - as described here - vice versa.
The cyclisation of ATP to cAMP does not provide 2 anorganic phosphates. Indeed, one molecule of pyrophosphate is produced.
cAMP may regulate the gene repressor of PKA. However, this cellular response would be far to slow. For fast response reactions the interaction of cAMP to regulatory subunits of PKA is important, resulating in the release of PKAs catalytic subunits. —Preceding unsigned comment added by 85.179.128.249 (talk) 15:25, 10 March 2008 (UTC)
[edit] ADH and Na retension
To explain a small (but important) edit I made...
Previously, the article stated that ADH retains water, but not salt. This is not entirely true.
ADH's primary function is indeed to increase water permeability in the collecting system. However, ADH also stimulates Na/K/Cl cotransport (in the thick asc. limb of loop of Henle), and stimulates apical Na channels in collecting tubules. Source: Boron & Boulpaep, Medical Physiology, Updated Ed., p. 787.
I have changed the page (removing the words "but not salt").
---bob (talk) 18:26, 21 March 2008 (UTC)
[edit] Camels
Do Camels have any sort of increased retention of ADH and that is how they save so much water? 76.14.97.253 (talk) 17:47, 4 April 2008 (UTC)
