Mathematical modeling suggests the tubuloglomerular feedback mechanism acts primarily via afferent arteriole resistance but is less efficient at autoregulating renal blood flow and GFR than other mechanisms.
Answers are grounded in this paper and cite their sources.
Does not support clinical TGF targeting; leaves open the relative efficiency of superficial nephron autoregulation in humans.
The effector site of the macula densa tubuloglomerular feedback mechanism was determined with a mathematical model of glomerular ultrafiltration. The feedback response was found to be mediated by an increase in the hydraulic resistance of the afferent arteriole, possibly accompanied by a slight decrease in the ultrafiltration coefficient of the glomerular membrane. The contribution of the tubuloglomerular feedback mechanism to the autoregulation of renal blood flow and GFR during increased arterial blood pressure was evaluated with a mathematical model of the kidney. The tubuloglomerular feedback system of the superficial nephron was found to be a less efficient regulator of renal blood flow and GFR than the remainder of the autoregulatory mechanism.
No takes yet. Share an insight, caveat, or question.
Jensen et al. (1982) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: