- Aldosterone increases the reabsorption of Na+ from the tubular fluid in the thick ascending limb of loop of Henle and in the distal tubule. These effects are explained in the following
proposed statements:
A. Aldosterone increases the number of Na+-Cl– symporter in the apical membrane of principal cells in the early portion of distal tubule
B. The number of Na+ channels (ENaC) is increased in the apical membrane of principal cells in the late portion of distal tubule by aldosterone
C. The synthesis of Na+, K+-ATPase in the basolateral portion of principal cells in distal tubule is
decreased by the action of aldosterone
D. Aldosterone increases the reabsorption of Na+ across the apical cell membrane in the thick
ascending limb of loop of Henle by decreasing Na+, K+-ATPase in it
Which one of the following combinations represents both correct statements?
(1) A and B (2) B and C
(3) C and D (4) A and D
Aldosterone, a key mineralocorticoid hormone secreted by the adrenal cortex, plays a vital role in regulating sodium (Na+) reabsorption in the kidneys, especially in the thick ascending limb of the loop of Henle and the distal tubule. This hormone’s actions are critical in controlling blood volume, blood pressure, and electrolyte balance.
Understanding Aldosterone’s Mechanism of Action
Upon binding to mineralocorticoid receptors inside principal cells of the distal nephron, aldosterone triggers transcriptional changes that increase the expression and activity of key sodium transport mechanisms. These include:
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Sodium-chloride symporters (NCC) in the distal convoluted tubule,
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Epithelial sodium channels (ENaC) in later sections,
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Basolateral sodium-potassium ATPase pumps that move sodium into the interstitial space and bloodstream.
Breakdown of the Proposed Statements:
Statement A:
Aldosterone increases the number of Na+-Cl- symporters in the apical membrane of principal cells in the early portion of the distal tubule.
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This is correct. Aldosterone upregulates the thiazide-sensitive Na+-Cl- cotransporter (NCC) in the early distal tubule, enhancing sodium reabsorption.wikipedia+1
Statement B:
The number of Na+ channels (ENaC) is increased in the apical membrane of principal cells in the late portion of the distal tubule by aldosterone.
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This is correct. Aldosterone stimulates the synthesis and insertion of ENaC channels specifically on the apical side of principal cells in the late distal tubule and collecting duct segments, allowing increased Na+ uptake.ncbi.nlm.nih+1
Statement C:
The synthesis of Na+, K+-ATPase in the basolateral portion of principal cells in distal tubule is decreased by the action of aldosterone.
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This is incorrect. Aldosterone increases the number and activity of Na+, K+-ATPase pumps on the basolateral membrane, facilitating the extrusion of reabsorbed sodium into the interstitial fluid and maintaining the gradient needed for Na+ reabsorption.pubmed.ncbi.nlm.nih+1
Statement D:
Aldosterone increases the reabsorption of Na+ across the apical cell membrane in the thick ascending limb of loop of Henle by decreasing Na+, K+-ATPase in it.
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This is incorrect. Aldosterone has a limited direct effect on the thick ascending limb. Moreover, Na+, K+-ATPase activity is generally enhanced (not decreased) to maintain the sodium gradient driving reabsorption. Aldosterone mainly acts in distal nephron segments rather than the thick ascending limb.wikipedia+1
Summary Table
Statement Description Correct/Incorrect A Upregulates Na+-Cl- symporters in early distal tubule Correct B Upregulates ENaC channels in late distal tubule Correct C Decreases Na+, K+-ATPase synthesis in principal cells Incorrect D Decreases Na+, K+-ATPase in thick ascending limb Incorrect Conclusion
The correct statements reflecting aldosterone’s effect on sodium reabsorption are:
(1) A and B
Aldosterone increases both the number of Na+-Cl- symporters (NCC) in the early distal tubule and sodium channels (ENaC) in the late distal tubule principal cells. It also stimulates—but does not decrease—Na+, K+-ATPase activity, and it has minimal effect on sodium transport in the thick ascending limb of the loop of Henle.
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