Tubuloglomerular feedback (TGF) is mediated by the macula densa sensing increased NaCl delivery. What is the final effector mechanism that reduces GFR?
- A Adenosine released from macula densa acts on A1 receptors causing afferent arteriolar vasoconstriction ✓
- B Angiotensin II released locally acts on efferent arterioles causing vasodilation
- C Prostaglandin E2 released causes afferent arteriolar vasodilation increasing GFR
- D Renin secreted by juxtaglomerular cells directly constricts the efferent arteriole
Explanation
When macula densa NaCl delivery increases, NKCC2-mediated transport rises, increasing intracellular [Na⁺] and ATP. Ecto-5'-nucleotidase converts AMP to adenosine in the interstitium. Adenosine acts on A1 receptors on the afferent arteriole causing vasoconstriction, reducing glomerular blood flow and GFR — a negative feedback restoring normal distal NaCl delivery. Macula densa cells also suppress renin release (via increased NaCl/adenosine) but this is a separate, slower mechanism via NO and PGE2.
Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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