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Controlled by

Target	Location	Function	Result
ENaC (Epithelial Na⁺ Channel)	Apical membrane	Increases Na⁺ entry from tubular lumen	↑ Na⁺ reabsorption
Na⁺/K⁺-ATPase	Basolateral membrane	Pumps 3 Na⁺ out (into blood) and 2 K⁺ in (into cell)	Maintains intracellular K⁺ for secretion; keeps lumen negative
ROMK (Renal Outer Medullary K⁺ Channel)	Apical membrane	Allows K⁺ to exit into lumen	↑ K⁺ secretion
H⁺-ATPase (in α-intercalated cells)	Apical membrane	H⁺ secretion	↑ acid secretion (metabolic alkalosis)

MOA

CCD → Cortical Collecting Duct

CCD → Cortical Collecting Duct

Aldosterone on K+

Aldosterone on K+

Control BP and K homeostasis
- Activated by RAA or !Hyperkalemia - ↑K (> 5)
- Increase K+ excretion
- Increase Na+ retention → increase blood volume → increase BP
*ACTH can stimulate aldosterone secretion acutely and transiently under normal conditions, but to a lesser extent than angiotensin II and potassium, and at lower doses than the ones needed for cortisol and DHEA production.

Effect:

Effect:

Up-regulating ENaC and ROMK at Cortical CD through gene expression (takes longer)
- Increased Na Sodium (135 - 145) re-absorption → Increased ECF → Increased blood volume, and blood pressure
Up-regulating and increasing the activity of H⁺/K⁺-ATPase at Cortical CD
- Ammoniagenesis: Create HCO3 - Bicarbs, Increased excretion of K Potassium (3.5-5) , Blood pH , and NH4+ - Ammonium form blood to urine

Affecting gene expression of: