Talk:Renin–angiotensin system

message: 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)
replies: text: 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)
thread_title: ANGIOTENSIN 2

message: 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)
thread_title:  Renal effects of angiotensin II 

message: 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. 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. 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. In diabetic patients who already had overt nephropathy, irbesartan and losartan slowed progression of the renal disease., 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)., The ARBs valsartan and candesartan have been shown to slow disease progression in patients with chronic heart failure (Val-HeFT, VALIANT, CHARM).,, Telmisartan was as effective as the ACE inhibitor ramipril in preventing cardiovascular events in high-risk hypertensive patients with diabetes or vascular disease (ONTARGET).
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)
thread_title:  Hypertension, treatment of 

message: 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)
replies: text: It just angiotensin 2 which is found in the lungs 129.180.166.53 (talk) 16:55, 9 June 2012 (UTC)
thread_title:  Conversion in the lungs 

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

message: 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)
thread_title:  Is angiotensinogen zymogen? 

message: gozUPwendehydrated,n?!?81.11.231.11 (talk) 05:21, 4 March 2016 (UTC)
thread_title:  a decrease in the filtrate NaCl concentration>RASactivates 

message: 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)
thread_title:  Cardiovascular effects PG acronym 

message: 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)
thread_title:  Should be a link to ACE2