Evidence map›Paper›PMID 22461303›Full record

ArticleAmerican journal of physiology. Renal physiology2012

Mechanisms of angiotensin II-enhanced connecting tubule glomerular feedback.

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

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Mechanisms of connecting tubule glomerular feedback enhancement by aldosterone.American journal of physiology. Renal physiology · 2016
    Article
  9. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  10. Article
  11. Intrarenal renin-angiotensin system in regulation of glomerular function.Current opinion in nephrology and hypertension · 2014
    Review
  12. Oxidative stress in hypertension: role of the kidney.Antioxidants & redox signaling · 2014
    Review
  13. Article
  14. Cell signaling through protein kinase C oxidation and activation.International journal of molecular sciences · 2012
    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

6 authors at 2 institutions in 1 country.

Yilin RenDivision of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Hospital, 2799 West Grand Blvd., Detroit, MI 48202, USA.
Martin A D'Ambrosio
Hong Wang
Edward L Peterson
Jeffrey L Garvin
Oscar A Carretero
Henry Ford Health System · USHenry Ford Hospital · US

Funding

VASOACTIVE HORMONES IN THE REGULATION OF BLOOD PRESSUREP01HL028982 · NHLBI · HENRY FORD HOSPITAL · PI PETERSON, EDWARD LAWRENCE · 1985 to 2017
$39.8M
Regulation of the Renal Microcirculation by the Connecting TubuleR01HL088036 · NHLBI · HENRY FORD HEALTH SYSTEM · PI CARRETERO, OSCAR A. · 2008 to 2012
$1.3M
NHLBI NIH HHS HL028982NHLBI NIH HHS HL088036NHLBI NIH HHS P01 HL028982NHLBI NIH HHS R01 HL088036
6 · The paper itself

Abstract

Increasing Na delivery to the connecting tubule (CNT) causes afferent arteriole (Af-Art) dilation, a process we call CNT glomerular feedback (CTGF). Angiotensin II (ANG II) in the CNT lumen enhances CTGF via PKC. We hypothesized that luminal ANG II stimulates CTGF via activation of protein kinase C (PKC), NADPH oxidase 2 (NOX2), and enhanced production of superoxide (O(2)(-)). Rabbit Af-Arts and adherent CNTs were microdissected and microperfused in vitro. Dilation of the Af-Art was induced by increasing luminal CNT NaCl from 0 to 5, 10, 30, 45, and 80 mM, and the concentration of NaCl that elicited a half-maximal response (EC(50)) was calculated. Compared with vehicle, adding ANG II (10(-9) M) to the CNT lumen reduced EC(50) from 37 ± 3 to 14 ± 1 mM (P < 0.001), indicating ANG II potentiates CTGF. In the presence of ANG II, the O(2)(-) scavenger tempol (10(-4) M) increased EC(50) from 20 ± 4 to 41 ± 3 mM (P < 0.01), the NOX inhibitor apocynin (10(-5) M) increased EC(50) from 17 ± 2 to 39 ± 4 mM (P < 0.01), and the specific NOX2 inhibitor gp91ds-tat (10(-5) M) increased EC(50) from 19 ± 2 to 34 ± 2 mM (P < 0.01). However, tempol, apocynin, and gp91ds-tat had no effect on CTGF in the absence of ANG II. Compared with vehicle, the PKC activator PMA (2 × 10(-7) M) decreased EC(50) from 35 ± 2 to 14 ± 1 (P < 0.001). In the presence of PMA, tempol increased EC(50) from 14 ± 2 to 35 ± 2 mM (P < 0.01). We conclude the PKC/NOX2/O(2)(-) pathway mediates the enhancement of CTGF by luminal ANG II but it does not participate in CTGF in the absence of ANG II.

Indexed as

Angiotensin IIAnimalsArteriolesFeedback, PhysiologicalKidney GlomerulusKidney TubulesModels, AnimalNADPH OxidasesProtein Kinase CRabbitsSignal TransductionSodium ChlorideSuperoxidesVasodilationAngiotensin IINADPH OxidasesProtein Kinase CSodium ChlorideSuperoxides

Identifiers

PMID22461303
PMCPMC3404582
OpenAlexW1969917516

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.