Role of a macula densa feedback mechanism as a mediator of renal autoregulation

Academic Article


  • The phenomenon of renal autoregulation demonstrates the presence of a sensitive intrarenal mechanism capable of maintaining GFR stable even during extrinsic disturbances that would be expected to alter renal hemodynamics. Substantial evidence has accumulated indicating that autoregulatory capability is dependent on the integrity of normal distal tubule flow dynamics and an intact distal tubuloglomerular feedback mechanism. Several whole-kidney and micropuncture studies have shown that interruption of volume delivery to the distal nephron interferes with autoregulation of renal blood flow (RBF) and GFR. The autoregulatory adjustments are probably localized at the afferent arterioles because the pressure in the larger arterioles does not exhibit autoregulation in response to decreases in renal perfusion pressure. It remains uncertain if the distal tubuloglomerular feedback mechanism is entirely responsible for autoregulatory responses. Data obtained in dog experiments indicate that under conditions of interrupted delivery to the distal nephron, SNGFR responses to decreases in arterial pressure are approximately those expected of a passive system where proximal tubule pressure is allowed to adjust to new steady-state levels with regard to the rapidity with which signals are transmitted to the distal nephron. Whole-kidney experiments indicate that, under conditions of a mild osmotic diuresis, the changes in urine flow following an increase in arterial pressure occur within 1 sec of the initiation of autoregulatory adjustments in vascular resistance. These experiments are consistent with the view that the major fraction of renal autoregulatory adjustments in resistance is mediated by the distal tubuloglomerular feedback mechanism that responds to some component of distal tubular flow and transmits signals to the afferent arteriolar segment of the same nephron.
  • Authors

    Published In

    Author List

  • Navar LG; Bell PD; Burke TJ
  • Volume

  • 22
  • Issue

  • Suppl. 12