Regarding the structure and functional characteristics of different nephron segments, all of the following are true EXCEPT:

Explanation

## Nephron Segments — Functional Hierarchy and Regulation ### Overview of Segment Functions **Key Point:** Different nephron segments have specialized structures and functions that work in concert to regulate fluid and electrolyte balance. The distal convoluted tubule (DCT) is **not** the primary site of aldosterone-mediated sodium reabsorption — that role belongs to the **collecting duct**. ### Functional Comparison Table | Segment | Water Permeability | Na^+^ Transport | Primary Regulation | % of Na^+^ Reabsorbed | | --- | --- | --- | --- | --- | | Descending LOH | High | Impermeable | Osmotic gradient | — | | Thick Ascending LOH | Impermeable | Active (NKCC2) | Metabolic | ~25% | | Distal Convoluted Tubule | Low (no ADH) | Active (NCC) | Thiazide-sensitive | ~5–10% | | Collecting Duct | Variable (ADH-dependent) | Active (ENaC) | **Aldosterone-dependent** | ~2–3% | ### Why the Incorrect Statement is Wrong **High-Yield:** The **collecting duct**, not the distal convoluted tubule, is the primary site of aldosterone-mediated sodium reabsorption and potassium secretion. Although the DCT does reabsorb some sodium via the thiazide-sensitive Na^+^-Cl^−^ cotransporter (NCC), aldosterone acts primarily on the principal cells of the collecting duct via mineralocorticoid receptors. **Clinical Pearl:** - **Aldosterone** → principal cells of collecting duct → epithelial sodium channel (ENaC) activation → Na^+^ reabsorption and K^+^ secretion - **Thiazide diuretics** block NCC in the DCT → mild hypokalemia (from increased distal K^+^ delivery) - **Aldosterone antagonists** (spironolactone) block collecting duct → hyperkalemia **Mnemonic:** **ALDO = Aldosterone Location = Distal collecting duct (not DCT)** ### Correct Statements Explained #### Descending Limb of Loop of Henle - Highly permeable to water via aquaporin-1 channels - Impermeable to NaCl (no active transport, tight junctions prevent paracellular diffusion) - Water reabsorption → tubular fluid becomes hypertonic - Concentration gradient drives passive NaCl entry in thick ascending limb #### Thick Ascending Limb of Loop of Henle - Active transport via **NKCC2** (Na^+^-K^+^-2Cl^−^ cotransporter) - **Impermeable to water** — this is the "diluting segment" - Reabsorbs ~25% of filtered sodium - Creates positive osmotic gradient in medullary interstitium (countercurrent multiplier) #### Collecting Duct - Permeability to water is **ADH-dependent** (aquaporin-2 insertion) - **ADH present** → aquaporin-2 insertion → water reabsorption → concentrated urine - **ADH absent** → impermeable to water → dilute urine - Aldosterone acts on principal cells → ENaC activation → Na^+^ reabsorption, K^+^ secretion **Warning:** Do not confuse the roles of DCT (thiazide-sensitive, modest Na^+^ reabsorption) and collecting duct (aldosterone-sensitive, fine-tuning of Na^+^ and K^+^). The DCT reabsorbs ~5–10% of filtered Na^+^; the collecting duct reabsorbs only ~2–3%, but this is under tight hormonal control.