Q.20 Which hormone primarily accelerates the reabsorption of Na• along the distal
convoluted tubule and proximal portion of collecting duct?
1.ADH
2.Renin
3.Aldosterone
4.Oxytocin
Aldosterone is the hormone that primarily accelerates Na⁺ reabsorption along the distal convoluted tubule (DCT) and proximal portion of the collecting duct.
Option Analysis
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ADH (Antidiuretic Hormone): Primarily increases water reabsorption in the collecting ducts by inserting aquaporin-2 channels into the apical membrane, but has minimal direct effect on Na⁺ reabsorption.
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Renin: An enzyme released by juxtaglomerular cells that initiates the renin-angiotensin-aldosterone system (RAAS), indirectly leading to aldosterone production, but does not directly act on tubules.
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Aldosterone: Correct answer. A mineralocorticoid from the adrenal cortex that binds mineralocorticoid receptors in principal cells of the late DCT and collecting duct, upregulating epithelial Na⁺ channels (ENaC) and Na⁺/K⁺-ATPase pumps to enhance Na⁺ reabsorption (about 2-3% of filtered load), followed by water.
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Oxytocin: Involved in uterine contraction and milk ejection; no role in renal ion reabsorption.
Aldosterone na reabsorption distal convoluted tubule collecting duct is a key topic in renal physiology for exams like NEET, GATE Life Sciences, and CSIR NET. This hormone regulates sodium balance to maintain blood pressure and fluid volume.
Mechanism of Aldosterone Action
Aldosterone binds mineralocorticoid receptors in principal cells of the late distal convoluted tubule (DCT) and cortical collecting duct. It increases ENaC channels on the apical membrane and Na⁺/K⁺-ATPase on the basolateral side, creating a gradient for Na⁺ entry from filtrate and exit to blood. This reabsorbs ~2% of filtered Na⁺, with water following osmotically, while promoting K⁺ secretion.
Why Not Other Hormones?
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ADH targets aquaporins for H₂O permeability in collecting ducts, not Na⁺ directly.
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Renin triggers RAAS but doesn’t act on tubules.
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Oxytocin has no renal ion role.
| Hormone | Primary Target | Na⁺ Reabsorption Effect |
|---|---|---|
| Aldosterone | Late DCT & Collecting Duct | Strongly increases via ENaC & Na⁺/K⁺-ATPase |
| ADH | Collecting Duct | Indirect (via water) |
| Renin | Plasma (enzyme) | None direct |
| Oxytocin | Uterus/Breast | None |
Clinical Relevance
In hypoaldosteronism, Na⁺ wasting causes hypotension; excess (hyperaldosteronism) leads to hypertension and hypokalemia. RAAS activation fine-tunes this in low volume states.
