Evidence map›Paper›PMID 18424635›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2008

Angiotensin II increases GABAB receptor expression in nucleus tractus solitarii of rats.

Fanrong Yao, Colin Sumners, Stephen T O'Rourke, Chengwen Sun

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.2field-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

24 citing papers in PubMed, 39 citations in OpenAlex.

  1. Article
  2. Loss of IP3R-BKInternational journal of molecular sciences · 2023
    Article
  3. Article
  4. Article
  5. GABA is a mediator of brain ATHypertension research : official journal of the Japanese Society of Hypertension · 2020
    Review
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Role of neurons and glia in the CNS actions of the renin-angiotensin system in cardiovascular control.American journal of physiology. Regulatory, integrative and comparative physiology · 2015
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
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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

4 authors at 1 institution in 1 country.

Fanrong YaoDepartment of Pharmaceutical Sciences, College of Pharmacy, North Dakota State University, Fargo, North Dakota, USA.
Colin Sumners
Stephen T O'Rourke
Chengwen Sun
North Dakota State University · US

Funding

TARGETING AND DELIVERYP20RR015566 · NCRR · NORTH DAKOTA STATE UNIVERSITY · PI DORSAM, GLENN PAUL · 2001 to 2011
$19.0M
Pilot Projects: Core DP30GM103332 · NIGMS · NORTH DAKOTA STATE UNIVERSITY · PI SIBI, MUKUND P. · 2012 to 2016
$4.9M
NCRR NIH HHS 2P20-RR-015566NCRR NIH HHS P20 RR015566NIGMS NIH HHS P30 GM103332
6 · The paper itself

Abstract

Increasing evidence indicates that both the angiotensin II (ANG II) and gamma-aminobutyric acid (GABA) systems play a very important role in the regulation of blood pressure (BP). However, there is little information concerning the interactions between these two systems in the nucleus tractus solitarii (NTS). In the present study, we examined the effects of ANG II on GABAA and GABAB receptor (GAR and GBR) expression in the NTS of Sprague-Dawley rats. The direct effect of ANG II on GBR expression was determined in neurons cultured from NTS. Treatment of neuronal cultures with ANG II (100 nM, 5 h) induced a twofold increase in GBR1 expression, as detected with real-time RT-PCR and Western blots, but had no effect on GBR2 or GAR expression. In electrophysiological experiments, perfusion of neuronal cultures with the GBR agonist baclofen decreased neuronal firing rate by 39% and 63% in neurons treated with either PBS (control) or ANG II, respectively, indicating that chronic ANG II treatment significantly enhanced the neuronal response to GBR activation. In contrast, ANG II had no significant effect on the inhibitory action of the GAR agonist muscimol. In whole animal studies, intracerebroventricular infusion of ANG II induced a sustained increase in mean BP and an elevation of GBR1 mRNA and protein levels in the NTS. These results indicate that ANG II stimulates GBR expression in NTS neurons, and this could contribute to the central nervous system actions of ANG II that result in dampening of baroreflexes and elevated BP in the central actions of ANG II.

Indexed as

BaroreflexBlood PressureAction PotentialsAngiotensin IIAnimalsAnimals, NewbornBaclofenBlotting, WesternCells, CulturedDisease Models, AnimalGABA AgonistsGABA-B Receptor AgonistsHypertensionInfusions, ParenteralMaleMuscimolAngiotensin IIBaclofenGABA AgonistsGABA-B Receptor AgonistsGabbr2 protein, ratMuscimolReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2Receptors, GABA-AReceptors, GABA-BRNA, Messenger

Identifiers

PMID18424635
PMCPMC4422374
OpenAlexW2108177961

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.