The tubuloglomerular feedback (TGF) mechanism regulates GFR locally. When GFR increases, tubular flow rises at the macula densa; the resulting vasomotor response and mediator are:

• A Afferent arteriolar dilation via renin release, forming angiotensin II locally
• B Efferent arteriolar constriction via increased aldosterone, reducing filtration pressure
• C Increased tubular NaCl reabsorption at macula densa reducing local osmolality signal
• D Afferent arteriolar constriction mediated by adenosine (and TxA2), reducing GFR back toward normal ✓

Explanation

Tubuloglomerular feedback (TGF) is a key intrarenal autoregulatory mechanism. When GFR rises, more NaCl is delivered to and sensed by macula densa cells (via NKCC2 cotransporter). Macula densa cells signal the adjacent juxtaglomerular apparatus to release adenosine (via ATP hydrolysis—ATP is released via pannexin channels and converted to adenosine extracellularly). Adenosine binds A1 receptors on afferent arterioles causing vasoconstriction, reducing glomerular capillary pressure and GFR. This negative feedback stabilizes GFR. Renin release is suppressed (not stimulated) by increased NaCl delivery. Thromboxane A2 may amplify afferent constriction but adenosine is the primary mediator. Efferent arteriole is not the primary target of TGF.

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

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