Evidence map›Paper›PMID 19325536›Full record

ArticleAmerican journal of hypertension2009

Angiotensin II regulation of renal vascular ENaC proteins.

Nikki L Jernigan, Joshua Speed, Babette LaMarca, Joey P Granger, Heather A Drummond

Open access · greenAbstract readComparative Study
In one paragraph

Article in American journal of hypertension, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. SECS, drugs, and Rac1&Rho: regulation of EnNaC in vascular endothelial cells.Pflugers Archiv : European journal of physiology · 2025
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Renal autoregulation in health and disease.Physiological reviews · 2015
    Review
  9. Article
  10. Pressure-induced constriction is inhibited in a mouse model of reduced betaENaC.American journal of physiology. Regulatory, integrative and comparative physiology · 2009
    Article
  11. Article
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

5 authors at 1 institution in 1 country.

Nikki L JerniganDepartment of Physiology and Biophysics, Center for Excellence in Cardiovascular-Renal Research, University of Mississippi Medical Center, Jackson, Mississippi, USA.
Joshua Speed
Babette LaMarca
Joey P Granger
Heather A Drummond
University of Mississippi Medical Center · US

Funding

STRUCTURAL VASCULAR ADAPTATION OF THE MICROCIRCULATIONP01HL051971 · NHLBI · UNIVERSITY OF MISSISSIPPI MEDICAL CENTER · PI HESTER, ROBERT L · 1993 to 2018
$39.4M
Vascular MechanosensorR01HL086996 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI DRUMMOND, HEATHER A · 2007 to 2010
$1.4M
ABNORMAL PRESSURE NATRIURESIS IN HYPERTENSIONR23HL033947 · NHLBI · MAYO CLINIC COLL OF MEDICINE, ROCHESTER · PI GRANGER, JOEY P. · 1985 to 1986
–
NHLBI NIH HHS HL33947NHLBI NIH HHS HL51971NHLBI NIH HHS HL86996NHLBI NIH HHS P01 HL051971NHLBI NIH HHS R01 HL086996
6 · The paper itself

Abstract

backgroundThe importance of beta and gamma epithelial Na(+) channel (ENaC) proteins in vascular smooth muscle cell (VSMC)-mediated pressure-induced constriction in renal interlobar arteries has been demonstrated recently. In renal epithelial tissue, ENaC expression is regulated by angiotensin II (Ang II). However, whether Ang II regulates vascular ENaC expression has never been determined. Therefore, the goal of the current investigation was to determine whether Ang II affects vascular ENaC expression and its contribution to pressure-induced constriction.

methodsTo address this goal, Sprague-Dawley rats were infused with Ang II (50 ng/kg/min) via osmotic minipump for 1 week. Mean arterial pressure (MAP) was measured using radiotelemetry. Interlobar arteries were isolated from these animals to assess VSMC ENaC protein expression, pressure-induced constriction, and agonist induced vascular reactivity.

resultsMAP was not different in control (113 +/- 2 mm Hg) and Ang II- (114 +/- 2 mm Hg) infused mice. We found that Ang II infusion decreased renal VSMC beta and gammaENaC immunolabeling by 18%. Consistent with this finding, we also found that ENaC-dependent peak pressure-induced constriction was inhibited from 38 +/- 3% to 25 +/- 1% at 125 mm Hg. Vasoreactivity to KCl, phenylephrine (PE), and acetylcholine (ACh) was unchanged.

conclusionsAng II suppression of pressure-induced constrictor responses in renal interlobar arteries may be mediated, at least in part, by inhibition of beta and gammaENaC protein expression.

Indexed as

Angiotensin IIAnimalsBlood PressureDisease Models, AnimalEpithelial Sodium ChannelsHypertension, RenovascularInfusions, IntravenousMaleMiceMuscle, Smooth, VascularRatsRats, Sprague-DawleyRenal ArteryVasoconstrictionVasoconstrictor AgentsAngiotensin IIEpithelial Sodium ChannelsVasoconstrictor Agents

Identifiers

PMID19325536
PMCPMC2787100
OpenAlexW2103921537

What OpenQuestion holds

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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.