RAAS Diagram
Draw RAAS diagrams of the renin-angiotensin-aldosterone system from renin release to angiotensin II and aldosterone, plus ACE inhibitor and ARB targets, heart failure and ACE2. Suited to physiology, pharmacology and nursing.
RAAS diagram examples
Real renders of the prompts shown: the full RAAS with the five actions of angiotensin II and its feedback loop, a seven-step overview, the drug targets and a blank version. Click one to load and edit its prompt.
From a fall in pressure to a rise in volume
Read top to bottom; each step is one box in the figure.
- 1
Trigger → renin
Low pressure or low NaCl makes the kidney release renin.
- 2
Angiotensin I → II
Renin and lung ACE turn liver angiotensinogen into angiotensin II.
- 3
Five effects via AT1
Vasoconstriction, aldosterone, ADH, thirst, sympathetic activity.
- 4
Feedback
Angiotensin II inhibits renin, the bar that closes the loop.
Where the four drug classes cut the chain
Each blocker is a bar on the step it stops.
- 1
ACE inhibitors
Bar on the ACE arrow: less angiotensin II is made.
- 2
ARBs
Bar between angiotensin II and its AT1 effects.
- 3
Renin and MR blockers
Aliskiren stops the first step; spironolactone the aldosterone arm.
RAAS diagrams for the kidney, the heart and the clinic
The figures above draw the classical cascade and the four drug classes on it, and the table below compares ACE inhibitors with ARBs. These are the other RAAS figures physiology, pharmacology and cardiology teaching draws; name the one you need.
Renin release at the juxtaglomerular apparatus
A close-up of the spot where the distal tubule touches its own glomerulus. Three inputs reach the renin-secreting granular (juxtaglomerular) cells in the afferent arteriole wall: less stretch of the arteriole, the intrarenal baroreceptor; less NaCl sensed by the macula densa through the NKCC2 cotransporter; and sympathetic stimulation of β1 receptors. The drug effects follow from it: loop diuretics block NKCC2, so the macula densa reads low NaCl and renin rises; β-blockers lower renin.
Angiotensin II effects organ by organ
One panel per organ instead of five boxes, all through the AT1 receptor. Arterioles: constriction. Kidney: the efferent arteriole constricts more than the afferent, holding up GFR when perfusion falls, and the proximal tubule reabsorbs more Na⁺ through the Na⁺/H⁺ exchanger. Adrenal zona glomerulosa: aldosterone. Brain: thirst and ADH release. Sympathetic nerve endings: more norepinephrine. Heart and vessel wall: hypertrophy and fibrosis over months. The efferent arm explains why GFR can fall sharply on an ACE inhibitor in bilateral renal artery stenosis.
Aldosterone in the principal cell
The slow arm at the level of one collecting duct cell. Aldosterone crosses the membrane and binds the mineralocorticoid receptor in the cytoplasm — draw it inside the cell, not on the surface; the complex enters the nucleus and raises ENaC on the luminal side and the Na⁺/K⁺-ATPase on the blood side, so Na⁺ is reabsorbed and K⁺ leaves through ROMK. 11β-HSD2 keeps cortisol off the receptor. Spironolactone and eplerenone block the receptor; amiloride blocks ENaC itself.
ACE, bradykinin and the ACE inhibitor cough
ACE is also kininase II, the enzyme that breaks down bradykinin. Draw it as one enzyme with two arrows — angiotensin I to angiotensin II, bradykinin to inactive fragments — and an ACE inhibitor bar across both: bradykinin builds up, which is the usual explanation for the dry cough and the rarer angioedema. ARBs leave ACE working. Add the feedback for both classes: renin rises with either, angiotensin II falls with an ACE inhibitor and rises with an ARB.
RAAS in heart failure
A loop rather than a line: falling cardiac output lowers renal perfusion, renin rises, and angiotensin II and aldosterone add volume and afterload and drive fibrosis and remodeling, which lower output further. The drugs that improve outcomes sit on that loop: ACE inhibitors or ARBs, the mineralocorticoid receptor antagonists spironolactone and eplerenone, and sacubitril/valsartan, an ARB paired with a neprilysin inhibitor so the natriuretic peptides last longer. Neprilysin also breaks down bradykinin, so sacubitril is never combined with an ACE inhibitor; a 36-hour washout comes first.
ACE2 and the angiotensin-(1–7) arm
The counter-regulatory side of the system, drawn as a second branch from angiotensin II, opposite the AT1 effects. ACE2, a carboxypeptidase, removes one amino acid from angiotensin II to give angiotensin-(1–7), which acts on the Mas receptor to dilate vessels and oppose fibrosis and inflammation; the AT2 receptor pulls the same way. ACE2 is also the receptor SARS-CoV-2 uses to enter cells, which is why it appears in COVID-19 figures.
Primary vs secondary hyperaldosteronism
Two columns that differ in renin. Primary aldosteronism, from an aldosterone-producing adenoma (Conn syndrome) or bilateral adrenal hyperplasia: aldosterone is high and renin suppressed, with hypertension and often hypokalemia; screening uses the aldosterone-to-renin ratio. Secondary hyperaldosteronism, as in renal artery stenosis, heart failure or cirrhosis: renin is high and drives the aldosterone.
What is the renin–angiotensin–aldosterone system?
The renin–angiotensin–aldosterone system (RAAS) is the hormone cascade that raises blood pressure and blood volume: when pressure falls, kidney juxtaglomerular cells release renin, which turns angiotensinogen from the liver into angiotensin I; angiotensin-converting enzyme (ACE), mainly in the lungs, turns that into angiotensin II, which constricts arterioles and releases aldosterone and ADH. Aldosterone makes the kidney keep Na⁺ and, with it, water.
Key facts
- Three signals release renin. Low pressure in the afferent arteriole, less NaCl reaching the macula densa, and sympathetic nerve stimulation through β-receptors all make juxtaglomerular cells secrete renin; circulating angiotensin II feeds back to suppress it.
- Renin and ACE are the two cutting steps. Renin cleaves angiotensinogen into the 10-amino-acid angiotensin I; ACE removes two more amino acids to give the active 8-amino-acid angiotensin II.
- Angiotensin II acts mainly through the AT1 receptor. Vasoconstriction, Na⁺ reabsorption and aldosterone secretion all run through AT1 — the receptor that ARBs block. Angiotensin II also triggers thirst, ADH release and sympathetic discharge.
- The fast arm and the slow arm. Angiotensin II raises pressure at once by vasoconstriction; aldosterone raises it more slowly by making the distal tubule and collecting duct reabsorb Na⁺ (water follows) and excrete K⁺.
- Four drug classes block the chain. Direct renin inhibitors (aliskiren) act on renin, ACE inhibitors (lisinopril) on ACE, angiotensin II receptor blockers (losartan) on the AT1 receptor and aldosterone receptor antagonists (spironolactone) on the aldosterone receptor; an ACE inhibitor and an ARB should not be combined.
Components of the renin–angiotensin–aldosterone system
The steps a labeled RAAS diagram is normally expected to show, where each one is made, what it does and what comes next. This is the default content unless you ask for something else.
| Component | Made in or released from | What it does | Next step |
|---|---|---|---|
| Macula densa | Distal tubule, at the juxtaglomerular apparatus | Senses less NaCl in the tubular fluid | Signals the juxtaglomerular cells |
| Renin | Juxtaglomerular cells of the afferent arteriole | Enzyme that cleaves angiotensinogen | Angiotensin I |
| Angiotensinogen | Liver | Inactive precursor circulating in plasma | Cut by renin |
| Angiotensin I | Blood plasma | Inactive 10-amino-acid peptide | Converted by ACE |
| ACE (angiotensin-converting enzyme) | Endothelium, mainly in the lungs | Converts angiotensin I into angiotensin II | Angiotensin II |
| Angiotensin II | Blood plasma | Constricts arterioles; releases aldosterone and ADH; triggers thirst and sympathetic discharge | AT1 receptors on vessels, adrenal cortex and brain |
| Aldosterone | Adrenal cortex | Na⁺ reabsorption (water follows) and K⁺ excretion in the distal tubule and collecting duct | Blood volume rises |
| ADH (vasopressin) | Posterior pituitary | Water reabsorption in the collecting duct; constricts peripheral vessels | Blood volume rises |
| Natriuretic peptides (ANP, BNP) | Heart atria and ventricles | Counter the RAAS: suppress renin, aldosterone and ADH | Blood pressure falls |
RAS and RAAS name the same system: renin–angiotensin system (RAS) stresses the renin → angiotensin steps, RAAS names aldosterone as well. Name the steps you need and only those are drawn.
ACE inhibitors vs ARBs: where does each act in the RAAS?
ACE inhibitors block the enzyme that turns angiotensin I into angiotensin II; angiotensin II receptor blockers (ARBs) let angiotensin II form but stop it acting on its AT1 receptor. Both lower blood pressure and both are first-line choices for hypertension, but they are not given together.
| ACE inhibitor | ARB | |
|---|---|---|
| Examples | Lisinopril, ramipril | Losartan |
| Step blocked | Angiotensin I → angiotensin II (ACE) | Angiotensin II → AT1 receptor |
| Where to draw the bar | On the ACE arrow | Between angiotensin II and its effects |
| Effect on the cascade | Less angiotensin II is made | Angiotensin II is made but cannot act through AT1 |
| Why one is swapped for the other | Cough or angioedema can make it intolerable | Used when an ACE inhibitor causes cough or angioedema |
| In pregnancy | Contraindicated | Contraindicated |
| Together | Not combined with an ARB | Not combined with an ACE inhibitor |
Two more drug classes act on the same chain: direct renin inhibitors such as aliskiren block renin at the top, and aldosterone receptor antagonists such as spironolactone block aldosterone at the bottom.
Common questions about the RAAS
How do I draw a RAAS diagram?
Start at the top with the trigger (low blood pressure), then draw the kidney releasing renin, renin turning angiotensinogen from the liver into angiotensin I, ACE in the lungs making angiotensin II, and angiotensin II fanning out to vasoconstriction, aldosterone, ADH and thirst, all converging on a rise in blood pressure. With this maker you describe the version you need and it is drawn top to bottom in that order.
What are the steps of the renin–angiotensin–aldosterone system?
Low pressure → juxtaglomerular cells release renin → renin converts angiotensinogen to angiotensin I → ACE converts angiotensin I to angiotensin II → angiotensin II constricts arterioles and releases aldosterone and ADH → the kidney keeps Na⁺ and water → blood volume and pressure rise. Rising angiotensin II then suppresses renin.
What triggers renin release?
A fall in pressure sensed in the afferent arteriole, less NaCl reaching the macula densa, and sympathetic stimulation through β-receptors. Angiotensin II itself inhibits renin release, closing the loop.
Where is ACE found?
Mainly on the endothelial cells of the lungs, which is where most angiotensin I is converted, but also in the kidneys and the brain. Most diagrams draw the lungs beside the ACE step.
What does angiotensin II do?
It constricts arterioles, stimulates the adrenal cortex to release aldosterone, releases ADH from the posterior pituitary, triggers thirst and increases sympathetic discharge. Together these raise blood volume and blood pressure.
What does aldosterone do in the RAAS?
Aldosterone makes the distal tubule and collecting duct reabsorb Na⁺ and excrete K⁺; water follows the sodium, so blood volume and pressure rise. It is the slow arm of the system, where angiotensin II vasoconstriction is the fast one.
Where do ACE inhibitors and ARBs act?
ACE inhibitors (lisinopril, ramipril) block the conversion of angiotensin I to angiotensin II; ARBs (losartan) block angiotensin II at its AT1 receptor. Direct renin inhibitors (aliskiren) act one step higher and aldosterone receptor antagonists (spironolactone) at the end of the chain.
How is the RAAS switched off?
By negative feedback: angiotensin II inhibits renin release, and as pressure and NaCl delivery recover the triggers disappear. Natriuretic peptides from the stretched heart also suppress renin, aldosterone and ADH.
Is renin a hormone or an enzyme?
Renin is an enzyme — a protease that cleaves angiotensinogen — although some sources call it a hormone because it is secreted into the blood and drives a hormone system. Diagrams usually draw it as the enzyme beside the angiotensinogen → angiotensin I arrow.
Why can ACE inhibitors and ARBs raise potassium and creatinine?
Less angiotensin II action means less aldosterone, so the collecting duct secretes less K⁺; and the efferent arteriole relaxes, so glomerular pressure and GFR fall. A small rise in creatinine after starting is expected; potassium and creatinine are checked within the first weeks, and the risk of hyperkalemia is highest with chronic kidney disease or alongside a mineralocorticoid receptor antagonist.
Sources
- Homeostatic Regulation of the Vascular System — Anatomy and Physiology 2e, section 20.4 — OpenStax
- Endocrine Regulation of Kidney Function — Anatomy and Physiology 2e, section 25.8 — OpenStax
- Hypertension — MSD Manual Professional Edition
- Metabolism of Angiotensinogen to Angiotensins (R-HSA-2022377) — Reactome
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