Tubuloglomerular Feedback

Overview
  • Tubuloglomerular Feedback is the principal mechanism which appears to be responsible for Autoregulation of GFR and RBF. The processes of tubuloglomerular feedback act as a negative feedback control mechanism which utilizes information regarding distal tubular fluid flow rate to control the Renal Blood Flow (RBF). Because the RBF ultimately affects the Glomerular Filtration Rate (GFR) and thus the distal fluid flow rate, tubuloglomerular feedback helps maintain a relatively stable value of RBF and GFR.
Mechanism
  • Overview
    • Like all negative feedback control circuits, tubuloglomerular feedback can be thought of as the coordinated action of a sensor, integrator, and effector.
  • Sensor: Macula Densa
    • The macula densa is a grouping of specialized tubular epithelial cells in the thick ascending loop of Henle that are positioned adjacent to the glomerulus. The macula densa senses the tubular fluid flow rate which for all intensive purposes is dependent and proportional to the GFR. The exact molecules whose flow is detected by the macula densa are not completely known although it is likely that they are sodium and chloride ions. Whatever the case, the macula densa sends this tubular flow information to the juxtaglomerular cells present in the walls of the renal afferent and efferent arterioles. It should be pointed out that the macula densa and juxtaglomerular cells are together known as the juxtaglomerular apparatus.
  • Integrator: Juxtaglomerular Cells
    • The juxtaglomerular cells are activated when the macula densa senses too little volume flow through the nephron, thus indicating a reduction in the GFR. In response, the juxtaglomerular cells initiate two processes which modulate the renal afferent and efferent arterioles. Juxtaglomerular cells appear to act directly on the renal afferent arterioles to cause their vasodilation. Additionally, juxtglomerular cells secrete renin which results in Angiotensin II release that in turn selectively causes vasoconstriction of the efferent arterioles.
  • Effectors: Renal Afferent and Efferent Arterioles
    • The coordinated effects on the renal afferent and efferent arterioles by the juxtaglomerular cells modulate the RBF in such a way as to increase glomerular capillary hydrostatic pressure. Vasodilation of the afferent arterioles reduces their resistance thus allowing more of the systemic arterial pressure to be conducted to the glomerulus, thus increasing the glomerular hydrostatic pressure. vasoconstriction of the efferent arterioles causes backup of blood into the glomerular capillaries, further contributing to increasing glomerular hydrostatic pressure. As described on the GFR page, boosting of the glomerular capillary hydrostatic pressure increases fluid filtration throgh the glomerulus and thus enhances the total GFR. With increased GFR, more fluid is delivered to the distal tubule, thus correcting any drop in fluid flow originally sensed by the macula densa. In this way, tubuloglomerular feedback helps maintain a relatively constant GFR and thus a distal tubular fluid flow rate.