AJP - Renal Physiology, Vol 259, Issue 4 715-F726, Copyright © 1990 by American Physiological Society
Model of TGF-proximal tubule interactions in renal autoregulation
W. A. Cupples, A. S. Wexler and D. J. Marsh
Department of Physiology and Biophysics, University of Southern California School of Medicine, Los Angeles 90033.
Previous models, assuming constant reabsorption in the proximal tubule,
have shown that tubuloglomerular feedback (TGF) can explain only a fraction
of glomerular filtration rate (GFR) and renal blood flow autoregulation.
Increased arterial pressure inhibits proximal tubule fluid reabsorption, an
effect that should increase the efficacy of TGF because of the resulting
increased flow rate in the loop of Henle. Models describing pressure and
flow in a glomerulus and a nephron were derived to test this prediction.
The models were coupled by a TGF function with tubular flow rate at the end
of the proximal tubule (superficial nephron) or at the macula densa
(juxtamedullary nephron) as input and with afferent arteriolar resistance
as output. In agreement with others, the model predicted that TGF alone
could account for about one-half of autoregulation. Pressure-dependent
inhibition of proximal reabsorption increased the ability of TGF to account
for autoregulation, providing compensation for increases in arterial
pressure comparable to published whole kidney values. The inclusion of an
approximation of an effect of arterial pressure on TGF marginally improved
predicted autoregulation. Although the results suggest that the proximal
tubule-TGF interaction can provide a quantitatively adequate explanation
for autoregulation, they also indicate that the effect of the interaction
is spent at arterial pressures greater than 130 mmHg. Additional mechanisms
are required to extend this range.
