Talk:Renin–angiotensin system

RAAS Schematic

ANGIOTENSIN 2

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)

I think that the figure (created/uploaded in 2006) isn't completely wrong as suggested in the comment above, if one notes the arrow pointing upward from aldosterone. It simply doesn't separate the activity of AT2 on Na reabsorption (in exchange for protons) from that of aldosterone in driving sodium/potassium exchange. I've created an SVG version using Inkscape and uploaded it to Commons to facilitate corrections. — soupvector (talk) 04:51, 19 February 2018 (UTC)

Terminology

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)

I'm sorry, but I have to agree (regarding "create", that is). "Angiotensin creates aldosterone" implies that the latter is directly derived from the former—that's not easier to understand, while it is inaccurate. Perhaps some compromise wording can be found, easier to understand while maintaining accuracy? Fvasconcellos (t·c) 17:29, 8 June 2008 (UTC)

Agreed, that should be easy to do I think. What confuses me was that the phrasing (of the older version) was "simple" in some places, while "advanced" in others, the mention of resistance with respect to the the afferent and efferent arterioles for instance. Wisdom89 _{(T / ^C)} 17:37, 8 June 2008 (UTC)

Perils of collaborative editing, I guess. Few articles have an internally consistent level of language when you look closely enough. Fvasconcellos (t·c) 17:53, 8 June 2008 (UTC)

Wisdom89, the reason I don't think they'd understand it is that I've talked to a lot of educated, intelligent cancer patients, and also to social workers and other non-clinical medical professionals, and I was surprised to find that they don't understand a lot of the words that you and I would take for granted.

Why do you think a layman would be able to understand the lead? Nbauman (talk) 18:10, 8 June 2008 (UTC)

Hmm, ok well, let's get specific for a moment so that we can discuss this in more depth. Which words do you feel are too obscure/arcane for the layperson? I feel that any confusing physiological terminology can and would be blue linked (e.g vascular resistance) Wisdom89 _{(T / ^C)} 01:34, 9 June 2008 (UTC)

Well, for example, "vascular resistance." Not only are the words difficult for the layman, but the concept is also difficult. In order to understand that sentence, you have to understand that vascular resistance causes pressure to increase. That's not a trivial or intuitive concept. Why should the pressure increase? I have a water pipe in my kitchen sink. If the water is flowing, and I increase the resistance, by tightening the faucet, the pressure doesn't increase. If I replace a low-resistance bulb in my light socket with a high-resistance bulb, the voltage doesn't increase. If you didn't already understand the physiology (and the physics) of the cardiovascular system, you wouldn't understand that sentence.

People often argue, "If the reader doesn't understand a technical term, they can always click on the Wikilink for an explanation." That doesn't work for several reasons. One reason is that when you click on the Wikilink, you usually get an explanation that just as difficult for a layman to understand as the one you started with. That's the case in Vascular resistance. It says, "Vascular resistance is a term used to define the resistance to flow that must be overcome to push blood through the circulatory system." That's saying, "Vascular resistance is vascular resistance." If you didn't know what vascular resistance was in the first place, that definition wouldn't help you. Nbauman (talk) 02:18, 10 June 2008 (UTC)

Renal effects of angiotensin II

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)

Hypertension, treatment of

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:

ANGIOTENSIN-CONVERTING ENZYME (ACE) INHIBITORS

ACE inhibitors are effective and well tolerated for treatment of hypertension. They may be less effective in black patients unless combined with a thiazide diuretic or calcium channel blocker. ACE inhibitors have been shown to prolong survival in patients with heart failure or left ventricular dysfunction after a myocardial infarction, reduce mortality in patients without heart failure or left ventricular dysfunction who are at high risk for cardiovascular events, and preserve renal function in patients with either diabetic or non-diabetic nephropathy.[1] In an open-label trial (ANBP2) among more than 6000 mostly white patients with a low incidence of diabetes, ACE inhibitor-treated male patients had an 11% lower incidence of cardiovascular events or all-cause mortality than those treated with various doses of thiazide diuretics (not assigned; up to the treating physician) despite similar reductions in blood pressure.[2] However, among 15,700 mostly white patients in the double-blind ALLHAT study, treatment of hypertension with an ACE inhibitor did not improve cardiovascular outcomes compared to chlorthalidone 12.5-25 mg. In black hypertensive participants in ALLHAT, the ACE inhibitor regimen was less effective than the diuretic in lowering blood pressure, and less effective in reducing stroke and cardiovascular events.

ANGIOTENSIN RECEPTOR BLOCKERS (ARBs)

ARBs are as effective in lowering blood pressure as ACE inhibitors, and appear to be equally reno- and cardioprotective, with fewer adverse effects. Irbesartan treatment delayed development of overt diabetic nephropathy in hypertensive patients with type 2 diabetes.[3] In diabetic patients who already had overt nephropathy, irbesartan and losartan slowed progression of the renal disease.[4],[5] In patients with hypertension and left ventricular hypertrophy, with or without diabetes (LIFE study group), losartan was more effective in decreasing cardiovascular morbidity and mortality, particularly from stroke, than a beta-blocker (atenolol).[6],[7] The ARBs valsartan and candesartan have been shown to slow disease progression in patients with chronic heart failure (Val-HeFT, VALIANT, CHARM).[8],[9],[10] Telmisartan was as effective as the ACE inhibitor ramipril in preventing cardiovascular events in high-risk hypertensive patients with diabetes or vascular disease (ONTARGET).[11]

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)

Conversion in the lungs

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)

It just angiotensin 2 which is found in the lungs 129.180.166.53 (talk) 16:55, 9 June 2012 (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)

Increasing cardiovascular response

Does angiotensin 2 increase cardiovascular response, based on HR*SV=CO? 129.180.166.53 (talk) 16:55, 9 June 2012 (UTC)

Is angiotensinogen zymogen?

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)

a decrease in the filtrate NaCl concentration>RASactivates

gozUPwendehydrated,n?!?81.11.231.11 (talk) 05:21, 4 March 2016 (UTC)

Cardiovascular effects PG acronym

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.

Should be a link to ACE2

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)