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2014 ; 306
(11
): F1357-71
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Theoretical assessment of renal autoregulatory mechanisms
#MMPMID24623150
Sgouralis I
; Layton AT
Am J Physiol Renal Physiol
2014[Jun]; 306
(11
): F1357-71
PMID24623150
show ga
A mathematical model of renal hemodynamics was used to assess the individual
contributions of the tubuloglomerular feedback (TGF) mechanism and the myogenic
response to glomerular filtration rate regulation in the rat kidney. The model
represents an afferent arteriole segment, glomerular filtration, and a short loop
of Henle. The afferent arteriole model exhibits myogenic response, which is
activated by hydrostatic pressure variations to induce changes in membrane
potential and vascular muscle tone. The tubule model predicts tubular fluid and
Cl(-) transport. Macula densa Cl(-) concentration is sensed as the signal for
TGF, which acts to constrict or dilate the afferent arteriole. With this
configuration, the model afferent arteriole maintains stable glomerular
filtration rate within a physiologic range of perfusion pressure (80-180 mmHg).
The contribution of TGF to overall autoregulation is significant only within a
narrow band of perfusion pressure values (80-110 mmHg). Model simulations of
ramp-like perfusion pressure perturbations agree well with findings by Flemming
et al. (Flemming B, Arenz N, Seeliger E, Wronski T, Steer K, Persson PB. J Am Soc
Nephrol 12: 2253-2262, 2001), which indicate that changes in vascular conductance
are markedly sensitive to pressure velocity. That asymmetric response is
attributed to the rate-dependent kinetics of the myogenic mechanism. Moreover,
simulations of renal autoregulation in diabetes mellitus predict that, due to the
impairment of the voltage-gated Ca(2+) channels of the afferent arteriole smooth
muscle cells, the perfusion pressure range in which single-nephron glomerular
filtration rate remains stable is reduced by ~70% and that TGF gain is reduced by
nearly 40%, consistent with experimental findings.
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