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Yo, its a mistake that AT2 increases the excretion of POTASIUM, please CORRECT THAT inda graphic, thanks —Preceding unsigned comment added by 200.45.157.109 ( talk) 08:10, 20 April 2011 (UTC)
The reason I reverted back to the other version was because a layman most definitely would be able to understand the syntax, terminology and wordage used in the article. Furthermore, some of the alternative terms were misleading; "created", for example, is extremely misleading, as none of these hormones/agents "creates" the other. I feel it should read "stimulates the releases of" which is correct in terms of endocrinology/physiology, and simply more accurate. Wisdom89 ( T / C) 17:21, 8 June 2008 (UTC)
Can anyone confirm that angiotensin II does increase the GFR and RBF through the nephron? My textbook claims (repeatedly) that it actually decreases GFR and RBF. —Preceding unsigned comment added by 211.28.151.54 ( talk) 07:09, 12 October 2008 (UTC)
Indeed, I think some of the information on this page may be misleading. Firstly, the distinction in the first paragraph should be made that it is in fact angiontensin II that stimulates most of these effects- "angiotensin" is a little vague considering angtiotensin I is believed to serve only as a precursor.
Secondly,though angiotensin II may act more on efferent than afferent arterioles ( thus + GFR), most textbooks indicate that the overall effect ( don't forget the significant effect on mesangial cells) is to -GFR. —Preceding unsigned comment added by 129.67.132.143 ( talk) 11:15, 3 May 2009 (UTC)
In the Clinical significance section, the first line reads "The renin-angiotensin system was often manipulated clinically to treat high blood pressure, but is no longer clinically relevant."
This is not supported by a reference, and there's a problem here.
The most recent issue of Treatment Guidelines (Volume 7, Number 77, published in January 2009) on "Drugs for Hypertension" has this to say about RAS manipulation:
Because Treatment Guidelines requires password access, the reader can't be linked directly to that publication, but if the online references in this quotation come through with proper function, it can be seen that the assertions made in these summary paragraphs are well-supported.
So why is it "no longer clinically relevant" to discuss the manipulation of the RAS in the management of high blood pressure? —Preceding unsigned comment added by 71.125.129.27 ( talk) 10:53, 26 August 2009 (UTC)
Angiotensin causes blood vessels to constrict Is this right? I do not think that it is the blood vessels that constrict but rather the arteries maybe, og the venes? —Preceding unsigned comment added by 192.38.111.186 ( talk) 19:03, 23 May 2010 (UTC)
Is this physiologically relevant? Is the relevant conversion, rather, done in the kidneys themselves? Seems like an inefficient system if conversion must be done in the lungs. —Preceding unsigned comment added by 67.193.129.101 ( talk) 13:36, 30 November 2010 (UTC)
"new evidence" that angiotensin 2 is found in all blood vessels links to an article from 1992. What? — Preceding unsigned comment added by 115.70.178.143 ( talk) 11:14, 3 October 2012 (UTC)
Does angiotensin 2 increase cardiovascular response, based on HR*SV=CO? 129.180.166.53 ( talk) 16:55, 9 June 2012 (UTC)
I don't think angiotensinogen is zymogen since angiotensin is hormone and not an enzyme. Is there any enzymatic reactivity to angiotensin that I'm not aware of? -- SongofSol ( talk) 20:00, 15 July 2014 (UTC)
gozUPwendehydrated,n?!? 81.11.231.11 ( talk) 05:21, 4 March 2016 (UTC)
Cardiovascular effects I want to know what PG refers to in the adjacent illustration. It seems entirely inappropriate to have a floating, undefined acronym with a clear medical meaning (prostaglandin) that is used in a different way. Presumably, since prostaglandin input to the RAS/RAAS system is not discussed in that section. ```` — Preceding unsigned comment added by 99.73.38.142 (talk) 04:27, 8 April 2020 (UTC) I signed it to attempt to make this clear. I can only say that this talk-page format is hands down the worst interface I have ever had to navigate. Swfowkes ( talk) 04:34, 8 April 2020 (UTC)
Addendum: I wrote to Ted Williams, the artist, and he said that PG does refer to prostaglandin. So I suggest that some prostaglandin content needs to be added to this page.
There should be a discussion of how angiotensin II is inactivated by ACE2. — Preceding unsigned comment added by Ribazole ( talk • contribs) 07:03, 10 February 2021 (UTC)
![]() | This article is rated C-class on Wikipedia's
content assessment scale. It is of interest to the following WikiProjects: | |||||||||||||
|
Yo, its a mistake that AT2 increases the excretion of POTASIUM, please CORRECT THAT inda graphic, thanks —Preceding unsigned comment added by 200.45.157.109 ( talk) 08:10, 20 April 2011 (UTC)
The reason I reverted back to the other version was because a layman most definitely would be able to understand the syntax, terminology and wordage used in the article. Furthermore, some of the alternative terms were misleading; "created", for example, is extremely misleading, as none of these hormones/agents "creates" the other. I feel it should read "stimulates the releases of" which is correct in terms of endocrinology/physiology, and simply more accurate. Wisdom89 ( T / C) 17:21, 8 June 2008 (UTC)
Can anyone confirm that angiotensin II does increase the GFR and RBF through the nephron? My textbook claims (repeatedly) that it actually decreases GFR and RBF. —Preceding unsigned comment added by 211.28.151.54 ( talk) 07:09, 12 October 2008 (UTC)
Indeed, I think some of the information on this page may be misleading. Firstly, the distinction in the first paragraph should be made that it is in fact angiontensin II that stimulates most of these effects- "angiotensin" is a little vague considering angtiotensin I is believed to serve only as a precursor.
Secondly,though angiotensin II may act more on efferent than afferent arterioles ( thus + GFR), most textbooks indicate that the overall effect ( don't forget the significant effect on mesangial cells) is to -GFR. —Preceding unsigned comment added by 129.67.132.143 ( talk) 11:15, 3 May 2009 (UTC)
In the Clinical significance section, the first line reads "The renin-angiotensin system was often manipulated clinically to treat high blood pressure, but is no longer clinically relevant."
This is not supported by a reference, and there's a problem here.
The most recent issue of Treatment Guidelines (Volume 7, Number 77, published in January 2009) on "Drugs for Hypertension" has this to say about RAS manipulation:
Because Treatment Guidelines requires password access, the reader can't be linked directly to that publication, but if the online references in this quotation come through with proper function, it can be seen that the assertions made in these summary paragraphs are well-supported.
So why is it "no longer clinically relevant" to discuss the manipulation of the RAS in the management of high blood pressure? —Preceding unsigned comment added by 71.125.129.27 ( talk) 10:53, 26 August 2009 (UTC)
Angiotensin causes blood vessels to constrict Is this right? I do not think that it is the blood vessels that constrict but rather the arteries maybe, og the venes? —Preceding unsigned comment added by 192.38.111.186 ( talk) 19:03, 23 May 2010 (UTC)
Is this physiologically relevant? Is the relevant conversion, rather, done in the kidneys themselves? Seems like an inefficient system if conversion must be done in the lungs. —Preceding unsigned comment added by 67.193.129.101 ( talk) 13:36, 30 November 2010 (UTC)
"new evidence" that angiotensin 2 is found in all blood vessels links to an article from 1992. What? — Preceding unsigned comment added by 115.70.178.143 ( talk) 11:14, 3 October 2012 (UTC)
Does angiotensin 2 increase cardiovascular response, based on HR*SV=CO? 129.180.166.53 ( talk) 16:55, 9 June 2012 (UTC)
I don't think angiotensinogen is zymogen since angiotensin is hormone and not an enzyme. Is there any enzymatic reactivity to angiotensin that I'm not aware of? -- SongofSol ( talk) 20:00, 15 July 2014 (UTC)
gozUPwendehydrated,n?!? 81.11.231.11 ( talk) 05:21, 4 March 2016 (UTC)
Cardiovascular effects I want to know what PG refers to in the adjacent illustration. It seems entirely inappropriate to have a floating, undefined acronym with a clear medical meaning (prostaglandin) that is used in a different way. Presumably, since prostaglandin input to the RAS/RAAS system is not discussed in that section. ```` — Preceding unsigned comment added by 99.73.38.142 (talk) 04:27, 8 April 2020 (UTC) I signed it to attempt to make this clear. I can only say that this talk-page format is hands down the worst interface I have ever had to navigate. Swfowkes ( talk) 04:34, 8 April 2020 (UTC)
Addendum: I wrote to Ted Williams, the artist, and he said that PG does refer to prostaglandin. So I suggest that some prostaglandin content needs to be added to this page.
There should be a discussion of how angiotensin II is inactivated by ACE2. — Preceding unsigned comment added by Ribazole ( talk • contribs) 07:03, 10 February 2021 (UTC)