Macula densa and tubuloglomerular feedback

Distal tubule · NKCC2 sensor Adenosine A1 Renin

Specialised plaque of cells where the thick ascending limb returns to touch its own glomerulus between the afferent and efferent arterioles. It senses NaCl delivery through NKCC2 and feeds back on afferent tone and renin release, completing the juxtaglomerular apparatus.

Traced from the start

  1. Glomerular filtration barrier
  2. Proximal tubule: Na+/H+ exchange and bicarbonate reclamation
  3. Thick ascending limb of Henle (NKCC2)
  4. Macula densa and tubuloglomerular feedback

Detail

Senses
Luminal NaCl concentration via NKCC2 uptake (normally ~20-60 mmol/L at this site)
High NaCl delivery
Macula densa releases ATP, converted to adenosine, which constricts the afferent arteriole through A1 receptors so GFR falls (negative feedback within ~10 s); renin release is suppressed
Low NaCl delivery
PGE2 and nitric oxide dilate the afferent arteriole and stimulate renin release from JG cells; angiotensin II then constricts the efferent and restores GFR
Function
With the myogenic response, TGF keeps GFR and distal delivery stable across MAP ~80-180 mmHg, protecting the limited distal Na+-reabsorbing capacity from being overwhelmed
Diuretic interaction
Loop diuretics block macula densa NKCC2: TGF is switched off (GFR does not fall despite the huge distal delivery) and renin release is stimulated

When it goes wrong

Early diabetes: SGLT2 upregulation raises proximal reabsorption and starves the macula densa of NaCl

Afferent dilatation and glomerular hyperfiltration, the first haemodynamic step toward diabetic nephropathy

SGLT2 inhibitor restoring distal NaCl delivery

TGF re-engages and afferent tone returns: intraglomerular pressure falls, giving an expected acute eGFR dip of ~3-5 mL/min followed by long-term renoprotection

NSAID plus ACE inhibitor or ARB plus diuretic ('triple whammy')

Loss of afferent dilatation, loss of efferent constriction and volume depletion combine to cause pre-renal acute kidney injury

Loop diuretic therapy

Macula densa-driven renin release adds secondary hyperaldosteronism to the K+ and H+ losses

Practise this structure

1 question in the bank tagged Glomerular Filtration.