Evidence map›Paper›PMID 22378773›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2012

Angiotensin II type 2 receptor-coupled nitric oxide production modulates free radical availability and voltage-gated Ca2+ currents in NTS neurons.

Gang Wang, Christal G Coleman, Michael J Glass, Ping Zhou, Qi Yu, Laibaik Park, Josef Anrather, Virginia M Pickel, Costantino Iadecola

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2012. 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 21% 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, 27 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Oxidative Stress and Hypertensive Diseases.The Medical clinics of North America · 2017
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Effects of nitric oxide on magnocellular neurons of the supraoptic nucleus involve multiple mechanisms.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014
    Review
  13. Article
  14. Article
  15. 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

9 authors at 1 institution in 1 country.

Gang WangDivision of Neurobiology, Department of Neurology and Neuroscience, Weill Cornell Medical College, New York 10065, USA. gaw2001@med.cornell.edu
Christal G Coleman
Michael J Glass
Ping Zhou
Qi Yu
Laibaik Park
Josef Anrather
Virginia M Pickel
Costantino Iadecola
Cornell University · US

Funding

Radiotelemetry CoreP01HL096571 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI DAVISSON, ROBIN L · 2009 to 2013
$8.8M
ULTRASTRUCTURE OF MESOLIMBIC TRANSMITTER INTERACTIONSR37MH040342 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI PICKEL, VIRGINIA M · 1988 to 2007
$2.5M
ULTRASTRUCTURE OF MESOLIMBIC TRANSMITTER INTERACTIONSR01MH040342 · NIMH · WEILL MEDICAL COLL OF CORNELL UNIV · PI PICKEL, VIRGINIA M · 1985 to 2012
$1.7M
NHLBI NIH HHS HL-096571NHLBI NIH HHS P01 HL096571NIMH NIH HHS MH-40342NIMH NIH HHS R01 MH040342NIMH NIH HHS R37 MH040342
6 · The paper itself

Abstract

The medial region of the nucleus tractus solitarius (mNTS) is a key brain stem site controlling cardiovascular function, wherein ANG II modulates neuronal L-type Ca(2+) currents via activation of ANG II type 1 receptors (AT(1)R) and production of reactive oxygen species (ROS). ANG II type 2 receptors (AT(2)R) induce production of nitric oxide (NO), which may interact with ROS and modulate AT(1)R signaling. We sought to determine whether AT(2)R-mediated NO production occurs in mNTS neurons and, if so, to elucidate the NO source and the functional interaction with AT(1)R-induced ROS or Ca(2+) influx. Electron microscopic (EM) immunolabeling showed that AT(2)R and neuronal NO synthase (nNOS) are coexpressed in neuronal somata and dendrites receiving synapses in the mNTS. In the presence of the AT(1)R antagonist losartan, ANG II increased NO production in isolated mNTS neurons, an effect blocked by the AT(2)R antagonist PD123319, but not the angiotensin (1-7) antagonist D-Ala. Studies in mNTS neurons of nNOS-null or endothelial NOS (eNOS)-null mice established nNOS as the source of NO. ANG II-induced ROS production was enhanced by PD123319, the NOS inhibitor N(G)-nitro-l-arginine (LNNA), or in nNOS-null mice. Moreover, in the presence of losartan, ANG II reduced voltage-gated L-type Ca(2+) current, an effect blocked by PD123319 or LNNA. We conclude that AT(2)R are closely associated and functionally coupled with nNOS in mNTS neurons. The resulting NO production antagonizes AT(1)R-mediated ROS and dampens L-type Ca(2+) currents. The ensuing signaling changes in the NTS may counteract the deleterious effects of AT(1)R on cardiovascular function.

Indexed as

AnimalsCalciumCalcium Channels, L-TypeCells, CulturedFree RadicalsIon Channel GatingMaleMiceMice, Inbred C57BLMice, KnockoutNitric OxideRatsRats, Sprague-DawleyReceptors, AngiotensinSolitary NucleusCalciumCalcium Channels, L-TypeFree RadicalsNitric OxideReceptors, Angiotensin

Identifiers

PMID22378773
PMCPMC3362142
OpenAlexW2140217309

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.