ArticleAmerican journal of physiology. Renal physiology2014
Salt sensitivity of tubuloglomerular feedback in the early remnant kidney.
Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
- Gut-derived uremic toxin handling in vivo requires OAT-mediated tubular secretion in chronic kidney disease.JCI insight · 2020Article
- Nitric oxide mediates anomalous tubuloglomerular feedback in rats fed high-NaCl diet after subtotal nephrectomy.American journal of physiology. Renal physiology · 2019Article
- Hypoxia-inducible factor-1α activation improves renal oxygenation and mitochondrial function in early chronic kidney disease.American journal of physiology. Renal physiology · 2017Article
- Renal Oxygenation in the Pathophysiology of Chronic Kidney Disease.Frontiers in physiology · 2017Review
- Recent advances in renal hemodynamics: insights from bench experiments and computer simulations.American journal of physiology. Renal physiology · 2015Review
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2 authors.
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Abstract
We previously reported internephron heterogeneity in the tubuloglomerular feedback (TGF) response 1 wk after subtotal nephrectomy (STN), with 50% of STN nephrons exhibiting anomalous TGF (Singh P, Deng A, Blantz RC, Thomson SC. Am J Physiol Renal Physiol 296: F1158-F1165, 2009). Presently, we tested the theory that anomalous TGF is an adaptation of the STN kidney to facilitate increased distal delivery when NaCl balance forces the per-nephron NaCl excretion to high levels. To this end, the effect of dietary NaCl on the TGF response was tested by micropuncture in STN and sham-operated Wistar rats. An NaCl-deficient (LS) or high-salt NaCl diet (HS; 1% NaCl in drinking water) was started on day 0 after STN or sham surgery. Micropuncture followed 8 days later with measurements of single-nephron GFR (SNGFR), proximal reabsorption, and tubular stop-flow pressure (PSF) obtained at both extremes of TGF activation, while TGF was manipulated by microperfusing Henle's loop (LOH) from the late proximal tubule. Activating TGF caused SNGFR to decline by similar amounts in Sham-LS, Sham-HS and STN-LS [ΔSNGFR (nl/min) = -16 ± 2, -11 ± 3, -11 ± 2; P = not significant by Tukey]. Activating TGF in STN-HS actually increased SNGFR by 5 ± 2 nl/min (P < 0.0005 vs. each other group by Tukey). HS had no effect on the PSF response to LOH perfusion in sham [ΔPSF (mmHg) = -9.6 ± 1.1 vs. -9.8 ± 1.0] but eliminated the PSF response in STN (+0.3 ± 0.9 vs. -5.7 ± 1.0, P = 0.0002). An HS diet leads to anomalous TGF in the early remnant kidney, which facilitates NaCl and fluid delivery to the distal nephron.
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