Evidence map›Paper›PMID 23220724›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback.

Qian Zhang, Lin Lin, Yan Lu, Haifeng Liu, Yanhua Duan, Xiaolong Zhu, Chengwei Zou, R Davis Manning, Ruisheng Liu

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.3field-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

8 citing papers in PubMed, 17 citations in OpenAlex.

  1. Dietary fructose enhances angiotensin II-stimulated NaAmerican journal of physiology. Renal physiology · 2020
    Article
  2. Article
  3. Effects of reactive oxygen species on renal tubular transport.American journal of physiology. Renal physiology · 2019
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Intrarenal renin-angiotensin system in regulation of glomerular function.Current opinion in nephrology and hypertension · 2014
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 2 countries.

Qian ZhangDepartment of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS 39216, USA.
Lin Lin
Yan Lu
Haifeng Liu
Yanhua Duan
Xiaolong Zhu
Chengwei Zou
R Davis Manning
Ruisheng Liu
University of Mississippi Medical Center · USShandong University · CN

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HESTER, ROBERT L · 1993 to 2018
$39.4M
Regulation of Superoxide Production by the Macula Densa during TGFR01HL086767 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI LIU, RUISHENG · 2007 to 2010
$1.7M
NHLBI NIH HHS HL-51971NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL086767NHLBI NIH HHS R01-HL-086767
6 · The paper itself

Abstract

Tubuloglomerular feedback (TGF)-mediated constriction of the afferent arteriole is modulated by a balance between release of superoxide (O(2)(-)) and nitric oxide (NO) in macula densa (MD) cells. Aldosterone activates mineralocorticoid receptors that are expressed in the MD and induces both NO and O(2)(-) generation. We hypothesize that aldosterone enhances O(2)(-) production in the MD mediated by protein kinase C (PKC), which buffers the effect of NO in control of TGF response. Studies were performed in microdissected and perfused MD and in a MD cell line, MMDD1 cells. Aldosterone significantly enhanced O(2)(-) generation both in perfused MD and in MMDD1 cells. When aldosterone (10(-7) mol/l) was added in the tubular perfusate, TGF response was reduced from 2.4 ± 0.3 μm to 1.4 ± 0.2 μm in isolated perfused MD. In the presence of tempol, a O(2)(-) scavenger, TGF response was 1.5 ± 0.2 μm. In the presence of both tempol and aldosterone in the tubular perfusate, TGF response was further reduced to 0.4 ± 0.2 μm. To determine if PKC is involved in aldosterone-induced O(2)(-) production, we exposed the O(2)(-) cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKCα inhibitor Go6976, or a PKCα siRNA, and the aldosterone-induced increase in O(2)(-) production was blocked. These data indicate that aldosterone-stimulated O(2)(-) production in the MD buffers the effect of NO in control of TGF response, an effect that was mediated by PKCα.

Indexed as

AldosteroneAnimalsBenzophenanthridinesCarbazolesEnzyme InhibitorsFeedback, PhysiologicalKidney GlomerulusKidney Tubules, DistalMaleModels, AnimalNitric OxideOxygenProtein Kinase C-alphaRabbitsReceptors, MineralocorticoidSuperoxidesAldosteroneBenzophenanthridinesCarbazoleschelerythrineEnzyme InhibitorsGo 6976Nitric OxideOxygenProtein Kinase C-alphaReceptors, MineralocorticoidSuperoxidesTransforming Growth Factors

Identifiers

PMID23220724
PMCPMC3566515
OpenAlexW2096853597

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.