tubuloglomerulaire

Tubuloglomerular refers to the tubuloglomerular apparatus and the tubuloglomerular feedback mechanism in the kidney. The system links the macula densa cells of the distal tubule to the afferent arteriole and glomerulus to regulate glomerular filtration rate (GFR) and sodium chloride delivery to the distal nephron.

Anatomy: The tubuloglomerular apparatus consists of the macula densa, a specialized group of tall, densely packed cells in the distal convoluted tubule; the afferent arteriole, which contains the juxtaglomerular (JG) cells; and extraglomerular mesangial cells. The macula densa senses luminal NaCl concentration and communicates with both the afferent arteriole and JG cells to modulate GFR and renin release.

Mechanism: When NaCl delivery to the macula densa is high, paracrine signals (notably adenosine) promote constriction of the afferent arteriole, reducing GFR. When NaCl delivery is low, signals diminish, leading to afferent dilation. Reduced NaCl delivery can also stimulate JG cells to release renin, activating the renin-angiotensin system; angiotensin II preferentially constricts the efferent arteriole, helping to maintain GFR. In this way, tubuloglomerular feedback adjusts filtration to stabilize GFR and NaCl delivery to the distal nephron.

Regulation and mediators: Adenosine-mediated signaling via A1 receptors is central to the afferent arm, with nitric oxide and prostaglandins modulating the response. Sympathetic input and the renin-angiotensin system influence JG cell activity and thus GFR control.

Clinical relevance: Tubuloglomerular feedback is essential for renal autoregulation. NSAIDs, which inhibit prostaglandin synthesis, can blunt the response; ACE inhibitors or ARBs reduce angiotensin II effects, altering efferent arteriolar tone and GFR. Diuretics that increase NaCl delivery to the macula densa can modify TGF sensitivity.