A patient is given furosemide. After achieving diuresis, which change in the tubular fluid reaching the macula densa ACTIVATES the tubuloglomerular feedback to reduce GFR?

• A Decreased NaCl delivery to the macula densa causing NKCC2-mediated renin release and GFR reduction
• B Increased NaCl delivery to the macula densa activating TGF and constricting the afferent arteriole ✓
• C Decreased tubular flow rate reducing tubular pressure and increasing GFR via Bowman's space pressure
• D Increased prostaglandin E2 from macula densa cells dilating the afferent arteriole after furosemide

Explanation

In normal TGF physiology, increased NaCl delivery to the macula densa (sensed via NKCC2 cotransport) triggers afferent arteriolar constriction, reducing GFR — a negative feedback protecting against excessive solute loss. Furosemide initially blocks NKCC2 and macula densa sensing, which releases TGF, allowing afferent arteriolar dilation and maintaining/increasing GFR while diuresis occurs. However, if NaCl delivery increases for other reasons, TGF activates to reduce GFR. The question asks about the activation stimulus for TGF, which is increased NaCl delivery (option B). Option A describes the opposite situation; option D is a local modulator but not the primary TGF activation signal.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.