Here's the full RAAS diagram! Let me walk you through the system so it clicks completely:
The RAAS Cascade - Step by Step
Step 1 - The Trigger (Kidney)
The juxtaglomerular (JG) cells in the kidney detect one of three signals:
- Low blood pressure
- Low sodium (Na+) in the filtrate
- Sympathetic nervous system activation (stress/blood loss)
They respond by releasing RENIN into the bloodstream.
Step 2 - Liver's Job
The liver constantly produces Angiotensinogen (an inactive precursor protein) and releases it into the blood.
Step 3 - Renin Acts
Renin is an enzyme that cleaves Angiotensinogen → Angiotensin I (still mostly inactive)
Step 4 - Lungs Activate It
As blood passes through the lungs, ACE (Angiotensin Converting Enzyme) on lung capillaries converts Angiotensin I → Angiotensin II (the powerful active form)
Step 5 - Angiotensin II Has 4 Major Effects:
| Target | Effect |
|---|
| Blood vessels | Vasoconstriction → raises BP directly |
| Adrenal cortex | Releases Aldosterone |
| Brain/Hypothalamus | Triggers thirst + ADH release |
| Kidney proximal tubule | Directly increases Na+ reabsorption |
Step 6 - Aldosterone (The Kidney's Final Act)
Aldosterone acts on the collecting duct and distal tubule to:
- Reabsorb Na+ (water follows osmotically)
- Excrete K+
- Result: increased blood volume → increased BP
Step 7 - Negative Feedback
Once blood pressure and volume are restored, renin secretion is suppressed - shutting the loop down.
Why it matters clinically: ACE inhibitors (like lisinopril) block Step 4, ARBs block Angiotensin II receptors, and spironolactone blocks aldosterone - all used to treat hypertension and heart failure.