Tubuloglomerular feedback (TGF) regulates GFR through the macula densa. When NaCl delivery to the macula densa increases, adenosine released from the macula densa acts on:

• A A1 receptors on afferent arteriole smooth muscle causing vasoconstriction and reducing GFR ✓
• B A2A receptors on efferent arteriole causing vasodilation and reducing GFR
• C A1 receptors on mesangial cells causing glomerular capillary contraction and reducing filtration surface area
• D A2B receptors on juxtaglomerular cells inhibiting renin secretion

Explanation

In tubuloglomerular feedback, increased NaCl at the macula densa triggers ATP release, which is rapidly converted to adenosine by ecto-5'-nucleotidase. Adenosine acts on A1 receptors on afferent arteriolar smooth muscle cells to cause vasoconstriction, increasing afferent arteriolar resistance and reducing glomerular hydrostatic pressure, thereby lowering GFR. This is a protective mechanism preventing excessive filtration when tubular flow is high. Prostaglandins counteract this by promoting afferent dilation, explaining why NSAIDs can acutely reduce GFR.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.