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Renin–Angiotensin–Aldosterone System (RAAS) is a critical hormonal cascade that regulates blood pressure, fluid balance, and electrolyte homeostasis. It plays a central role in the pathophysiology of hypertension, heart failure, and renal diseases like renovascular hypertension and chronic kidney disease (CKD).

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The Renin Angiotensin Aldosterone System (RAAS)

Overview of RAAS

Component Source Function
Renin Juxtaglomerular (JG) cells of kidney Converts angiotensinogen to angiotensin I
Angiotensinogen Liver Inactive precursor; substrate for renin
Angiotensin I Blood plasma Inactive; converted to angiotensin II
Angiotensin-Converting Enzyme (ACE) Lungs & vascular endothelium Converts angiotensin I → angiotensin II
Angiotensin II Blood plasma Potent vasoconstrictor, stimulates aldosterone
Aldosterone Adrenal cortex (zona glomerulosa) Promotes Na⁺ and water reabsorption, K⁺ excretion in kidneys

RAAS Cascade

  1. Trigger: ↓ blood pressure, ↓ renal perfusion (e.g., in renal artery stenosis), or ↓ Na⁺ at the macula densa
  2. Renin release from JG cells
  3. Renin cleaves angiotensinogen → angiotensin I
  4. ACE converts angiotensin I → angiotensin II
  5. Angiotensin II:
  6. Aldosterone → ↑ Na⁺ and water reabsorption in the distal nephron → ↑ blood volume

Physiological Effects

Target Effect of RAAS Activation
Blood vessels Vasoconstriction → ↑ systemic vascular resistance
Kidneys Na⁺/H₂O retention, K⁺ excretion → ↑ blood volume
Adrenal gland Aldosterone secretion
Brain Stimulates thirst, ↑ ADH secretion
Heart May contribute to remodeling and hypertrophy (chronic activation)

Laboratory Evaluation

Test Purpose
Plasma renin activity (PRA) Assess renin levels
Serum aldosterone Elevated in primary hyperaldosteronism or RAAS activation
Aldosterone-to-renin ratio (ARR) Key screen for primary aldosteronism

Pathological States