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🧪 Aldosterone Escape Phenomenon Lab

Explore why chronic aldosterone excess does not cause endless sodium retention: simulate pressure natriuresis, atrial natriuretic peptide, and the split between sodium escape and persistent potassium wasting.

Medical Technology & Imaging Physics3DModerate60 FPS

The simulator demonstrates how sustained aldosterone excess produces an initial period of positive sodium balance, volume expansion, and rising blood pressure, followed by a counter-regulatory plateau driven by pressure natriuresis and atrial natriuretic peptide, in which sodium excretion realigns with intake while blood pressure remains elevated and potassium excretion continues unabated.

🔬 What It Demonstrates

🎮 How to Use

Set a sustained mineralocorticoid (aldosterone) level and a fixed daily sodium intake, then run the simulation across several simulated days. Watch sodium balance, extracellular volume, and blood pressure rise initially, then observe the pressure natriuresis and atrial natriuretic peptide indicators activate as pressure climbs, driving sodium excretion back up to match intake. Compare the sodium balance curve, which plateaus, against the potassium balance curve, which keeps declining, to see the escape asymmetry directly. Try adjusting renal perfusion pressure sensitivity to see how blunting pressure natriuresis delays or weakens escape.

💡 Did You Know?

Classic experiments establishing aldosterone escape used constant high-dose mineralocorticoid infusion in animals on a fixed sodium diet: after about three to five days of weight gain from fluid retention, body weight and sodium balance plateaued completely, even though the mineralocorticoid dose never changed, while serum potassium kept falling throughout the entire experiment.

⚙ Under the hood

aldosteronerenal physiologysodium balancepressure natriuresishyperaldosteronismpotassium wastingraasendocrinology

3D · Three.js / WebGL renderer · 60 FPS target · runs fully client-side, no install