Talk:Endothelium-derived relaxing factor

EDRF = Nitric Oxide ?

IMHO, Nitric Oxide is an EDRF. The endothelium can release other vasorelaxing factors. Hopefully, someone would add these non-NO endothelium-derived vasorelaxing factors to this Wikipage even though they are not usually called EDRF. One example would be prostacyclin. (I might do this later....) -- PFHLai 20:36, 2004 Jun 3 (UTC)

I simply changed the wording, but the point already was that EDRF is synonymous with nitric oxide. Please expand if you think that prostacyclin (I have written eicosanoid, but not prostacyclin yet) belongs here. JFW | T@lk 23:06, 3 Jun 2004 (UTC)

It's true that EDRF is practically synonymous with Nitric Oxide (NO) even though it's not accurate -- it's like heart attack and heart failure, it will be hard to find too many people who care about the difference. NO has all the properties of EDRF as originally characterized by Furchgott, but NO is just one of the endothelial-derived compounds that acts as a vasorelaxant, i.e. an EDRF. Besides PGI2 (prostacyclin, which deserves its own Wikispace), there is carbon monoxide from heme oxygenases, but it is much, much, much weaker than NO as an EDRF. And there is also the enigmatic endothelial-derived hyperpolarizing factor, which may be short-lived compounds (I forgot their names, but I think one of them is called EET, not to be confused with ET the vasoconstrictor) generated by some P-450 cytochrome enzymes similar to cyclooxygenases .... Fun stuffs to read, but tough to fully comprehend ... (at least to my feeble mind.) Even tougher is for me to find anything in my messy office. I want to be sure of things before I start typing. If I can find those papers again, there will be additions made to this somewhat stubby Wikipage on EDRF. If I can find those papers ..... -- PFHLai 17:40, 2004 Jun 4 (UTC)

I believe EDRF should be considered synonymous with NO. When EDRF was discovered, it reflected the action of a single vasorelaxant substance with a short half-life. The actions of prostacyclin were already well known before EDRF was discovered to be NO. I don't think this article should include a description of any of the other relaxing factors. However, if you really wish to do this, the article would have to be called 'Endothelium-derived relaxing factors' (emphasis on plural), since you've already pointed out that there is more than one EDRF. In citing EDHF, you do make a good point though about whether this article should describe the other known relaxing factors. Usually vascular biologists call endothelium-derived hyperpolarizing factor to stage when they observe a relaxation that persists even under the blockade of eNOS and COX. EDHF is usually refered to as singular, even though its actions have been ascribed among others to epoxyeicosatrienoic acids (EETs), potassium ions released from endothelial cells, or even the presence of myoendothelial gap junctions. My point is that at the moment the knowledge about the precise identity of EDHF is sketchy to say the least. On the other hand EDRF is a factor that was once as impartially understood as EDHF, however all of its actions and properties could later be ascribed to NO. This cannot be said for EDHF, seeing its very heterogenous characterization. An article about EDHF should however include the many different substances and processes to which its action is ascribed. --Zorpidus 17:17, 12 Dec 2004 (UTC)

Is heme oxygenase and carbon monoxide considered an EDRF? I agree for practical terms of this article that EDRF has become synonymous with NO. I believe at my last inquiry EDHF was related to cannibanoid like metabolites or cytochrome P450 metabolites. GetAgrippa 04:01, 7 September 2006 (UTC)[reply]

I took out the reference to Minoxidil. It has nothing to do with EDRF and the mechanism of action in hair growth is still unknown. Minoxidil acts on ATP-sensitive potassim channels. EDRF works through altering calcium, actin-focal adhesion dynamics, and activating phosphatases just to mention the major.GetAgrippa 04:19, 7 September 2006 (UTC)[reply]

Minoxidil

"The putative nitric oxide agonist minoxidil [1] both dialates blood vessels and stimulates hair growth". This statment is ill founded so I removed it, again. Minoxidil works on ATP sensitive potasium channels. NO stimultes cGMP and then PKG. This alters L type calcium channels, calcium sensitive postassium channels, calcium pumps and phospholamban and phospholemman, calcium desensitization by altering myosin light chain phosphorylation, phosphorylation of a small heat shock protein which correlates with force suppression, etc. In fact, the small heat shock protein connection is a growing primary focus of vasodilation. I could find no peer reviewed publication connecting Minoxidil with NO, cGMP, or PKG. NO does not simply alter potassum channels as the reference would suggest. I would hope this would put this issue to rest. GetAgrippa 16:15, 21 September 2006 (UTC)[reply]