Step by Step
RAAS
The renin-angiotensin-aldosterone system
Low blood pressure, low sodium, or reduced renal perfusion triggers juxtaglomerular cells to release renin. Renin cleaves angiotensinogen into angiotensin I, which ACE (in the lungs) converts to angiotensin II — causing vasoconstriction and stimulating aldosterone release, ultimately raising blood pressure through sodium retention and increased blood volume. ACE inhibitors block this pathway.
Aldo
Aldosterone
Released from the adrenal cortex, aldosterone promotes sodium reabsorption (with potassium excretion) in the DCT and collecting duct — water follows the sodium, raising blood pressure. Spironolactone blocks this hormone.
ADH
ADH (vasopressin)
Released from the posterior pituitary in response to increased plasma osmolarity or decreased blood volume, ADH promotes aquaporin-2 insertion in the collecting duct, retaining water and concentrating urine. SIADH (syndrome of inappropriate ADH) refers to excessive ADH secretion.
ANP
ANP (atrial natriuretic peptide)
Released from the heart in response to increased atrial stretch (from high blood volume), ANP inhibits RAAS and aldosterone, promoting sodium excretion and ultimately lowering blood pressure — essentially working in the opposite direction from the other three hormones.
Applied Walkthrough
1
A patient with low blood pressure triggers the RAAS cascade: renin release leads to angiotensin II formation, which both directly vasoconstricts and stimulates aldosterone release.
2
Aldosterone then promotes sodium reabsorption in the kidney's DCT and collecting duct, with water following osmotically — together with the vasoconstriction from angiotensin II, this raises blood pressure back toward normal.
3
Simultaneously, if this same patient's blood volume was already somewhat low, increased plasma osmolarity would also trigger ADH release, further promoting water retention via aquaporin-2 insertion in the collecting duct.
4
By contrast, a patient with excess blood volume (causing increased atrial stretch) would release ANP instead — working in the opposite direction, inhibiting RAAS and aldosterone to promote sodium excretion and lower blood pressure back down.
Exam Application
Exams test whether you can trace the full RAAS cascade, distinguish aldosterone's action from ADH's action, and recognize ANP as the counter-regulatory hormone that opposes the other three by promoting sodium and water excretion rather than retention.
⚠ Common Trap
The most common trap is confusing aldosterone's target (sodium reabsorption, with water following osmotically) with ADH's target (direct water reabsorption via aquaporins) — both raise blood volume, but through different direct mechanisms.
✓ Quick Self-Check
1. What triggers renin release, and what is the ultimate downstream effect?
Low blood pressure, low sodium, or reduced renal perfusion; ultimately, vasoconstriction and increased blood volume (raising blood pressure).
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2. What does aldosterone directly promote in the kidney?
Sodium reabsorption (with potassium excretion) in the DCT and collecting duct.
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3. What does ADH directly promote in the kidney?
Water reabsorption via aquaporin-2 insertion in the collecting duct.
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4. What triggers ANP release, and what does it do?
Increased atrial stretch (from high blood volume); it inhibits RAAS and aldosterone, promoting sodium excretion and lowering blood pressure.
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5. What condition results from excessive ADH secretion?
SIADH (syndrome of inappropriate ADH).
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