Evidence map›Paper›PMID 23959547›Full record

ArticleHypertension (Dallas, Tex. : 1979)2013

Connecting tubule glomerular feedback in hypertension.

Hong Wang, Martin A D'Ambrosio, Jeffrey L Garvin, Yilin Ren, Oscar A Carretero

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 18% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 23 citations in OpenAlex.

  1. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  2. Article
  3. Rare Variants in Genes Encoding Subunits of the Epithelial NaHypertension (Dallas, Tex. : 1979) · 2022
    Article
  4. Renal blood flow and oxygenation.Pflugers Archiv : European journal of physiology · 2022
    Review
  5. Decreased tubuloglomerular feedback response in high-fat diet-induced obesity.American journal of physiology. Renal physiology · 2022
    Article
  6. Review
  7. Tubule-vascular feedback in renal autoregulation.American journal of physiology. Renal physiology · 2019
    Review
  8. Review
  9. Role of connecting tubule glomerular feedback in obesity related renal damage.American journal of physiology. Renal physiology · 2018
    Article
  10. Article
  11. Article
  12. Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017
    Review
  13. Article
  14. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  15. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Hong WangHypertension and Vascular Research Division, Department of Internal Medicine, Henry Ford Hospital, 2799 West Grand Blvd, Detroit, MI 48202. ocarret1@hfhs.org.
Martin A D'Ambrosio
Jeffrey L Garvin
Yilin Ren
Oscar A Carretero
Henry Ford Hospital · US

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI ORTIZ, PABLO A. · 1985 to 2017
$39.8M
NHLBI NIH HHS HL028982-31NHLBI NIH HHS P01 HL028982
6 · The paper itself

Abstract

In Dahl salt-sensitive rats (Dahl SS), glomerular capillary pressure increases in response to high salt intake and this is accompanied by significant glomerular injury compared with spontaneously hypertensive rats with similar blood pressure. Glomerular capillary pressure is controlled mainly by afferent arteriolar resistance, which is regulated by the vasoconstrictor tubule glomerular feedback (TGF) and the vasodilator connecting TGF (CTGF). We hypothesized that Dahl SS have a decreased TGF response and enhanced TGF resetting compared with spontaneously hypertensive rats, and that these differences are attributable in part to an increase in CTGF. In vivo, using micropuncture we measured stop-flow pressure (a surrogate of glomerular capillary pressure). TGF was calculated as the maximal decrease in stop-flow pressure caused by increasing nephron perfusion, TGF resetting as the attenuation in TGF induced by high salt diet, and CTGF as the difference in TGF response before and during CTGF inhibition with benzamil. Compared with spontaneously hypertensive rats, Dahl SS had (1) lower TGF responses in normal (6.6±0.1 versus 11.0±0.2 mm Hg; P<0.001) and high-salt diets (3.3±0.1 versus 10.1±0.3 mm Hg; P<0.001), (2) greater TGF resetting (3.3±0.1 versus 1.0±0.3 mm Hg; P<0.001), and (3) greater CTGF (3.4±0.4 versus 1.2±0.1 mm Hg; P<0.001). We conclude that Dahl SS have lower TGF and greater CTGF than spontaneously hypertensive rats, and that CTGF antagonizes TGF. Furthermore, CTGF is enhanced by a high-salt diet and contributes significantly to TGF resetting. Our findings may explain in part the increase in vasodilatation, glomerular capillary pressure, and glomerular damage in SS hypertension during high salt intake.

Indexed as

AmilorideAnimalsBlood PressureHypertensionKidney GlomerulusNephronsRatsRats, Inbred DahlVasoconstrictionAmiloridebenzamilbenzamilCTGFDahl salt-sensitive ratsrats, inbred SHRTGF

Identifiers

PMID23959547
PMCPMC3867812
OpenAlexW2125113680

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.