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Human Body Study

RAAS — Renin–Angiotensin–Aldosterone System

The renin–angiotensin–aldosterone system Low blood pressure, low sodium delivery, or sympathetic activation triggers kidney JG cells to release renin. Renin cleaves liver-made angiotensinogen into angiotensin I, which is converted in the lung by ACE into angiotensin II. Angiotensin II directly causes vasoconstriction, stimulates thirst, and drives AVP release, and also stimulates aldosterone release from the adrenal cortex. Aldosterone acts on the distal nephron to retain sodium and water and excrete potassium, raising blood pressure and volume — closing the feedback loop by suppressing further renin release. Triggered by: ↓ blood pressure · ↓ Na⁺ delivery · sympathetic activation Liver supplies angiotensinogen Kidney JG cells → renin Lung supplies ACE Angiotensinogen (circulating substrate) Angiotensin I Angiotensin II (active effector) Adrenal cortex zona glomerulosa Distal nephron · vasculature ↑ Na⁺ + water retention · ↑ K⁺ excretion (aldosterone) vasoconstriction · thirst · AVP release (AT-II direct) renin renin → ACE ACE → stimulates aldosterone AT-II direct effects Net: ↑ blood pressure · ↑ effective circulating volume restored BP/volume → ↓ renin K⁺ directly stimulates aldosterone independent of AT-II. ACE inhibitors, ARBs, and MR antagonists all target this axis.

Signaling chain

Section titled “Signaling chain”

A multi-organ cascade independent of the pituitary:

  1. Renin released by the kidney’s juxtaglomerular cells in response to low blood pressure, low sodium delivery, or sympathetic activation.
  2. Renin cleaves liver-derived angiotensinogen → angiotensin I.
  3. ACE (mainly in the lung) converts angiotensin I → angiotensin II.
  4. Angiotensin II stimulates aldosterone release from the adrenal cortex (zona glomerulosa).

Function

Section titled “Function”

The body’s principal regulator of blood pressure and sodium/fluid balance. Angiotensin II is a potent vasoconstrictor and stimulates thirst and AVP release. Aldosterone promotes renal sodium (and water) retention and potassium excretion in the distal nephron.

Feedback

Section titled “Feedback”

Restored blood pressure, volume, and sodium delivery suppress renin release, closing the loop. Potassium directly stimulates aldosterone independently of angiotensin II.

Clinical relevance

Section titled “Clinical relevance”
  • Hypertension — RAAS is a primary drug target: ACE inhibitors, ARBs, direct renin inhibitors, mineralocorticoid-receptor antagonists.
  • Primary hyperaldosteronism (Conn’s) — hypertension with hypokalemia; suppressed renin, high aldosterone.
  • Secondary activation — heart failure, cirrhosis, renal artery stenosis.
  • Drives adverse cardiac/renal remodeling in chronic disease.

Key labs

Section titled “Key labs”

Plasma renin activity, aldosterone, aldosterone-to-renin ratio (screen for Conn’s), serum potassium and sodium.