The reasoning: small fraction, decisive control
- DCT (~5–10% of Na⁺): apical NCC (thiazide target), TRPM6 Mg²⁺ entry, TRPV5 Ca²⁺ entry (PTH‑stimulated); WNK–SPAK kinases regulate NCC (Gordon syndrome/FHHt — hyperkalaemic hypertension, thiazide‑responsive).
- Connecting tubule and collecting duct principal cells: apical ENaC Na⁺ entry (aldosterone via MR → SGK1 → inhibition of NEDD4‑2), creating lumen‑negative voltage that drives K⁺ secretion via ROMK (basal) and BK (flow‑stimulated) channels; AQP2 (ADH).
- Intercalated cells: type A — apical H⁺‑ATPase and H⁺/K⁺‑ATPase, basolateral AE1 (acid secretion, K⁺ reabsorption); type B — apical pendrin (HCO₃⁻ secretion, Cl⁻ reabsorption).