Evidence map›Paper›PMID 37102686›Full record

ArticleAmerican journal of physiology. Renal physiology2023

A novel functional role for the classic CNS neurotransmitters, GABA, glycine, and glutamate, in the kidney: potent and opposing regulators of the renal vasculature.

Scott S Wildman, Kadeshia Dunn, Justin P Van Beusecum, Edward W Inscho, Stephen Kelley, Rebecca J Lilley, Anthony K Cook, Kirsti D Taylor, Claire M Peppiatt-Wildman

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 22% 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

7 citing papers in PubMed, 1 synthesis or guideline pooled it, 9 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. 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 3 institutions in 2 countries.

Scott S WildmanNortheastern University London, London, United Kingdom.
Kadeshia DunnDivision of Natural Sciences, University of Kent, Kent, United Kingdom.
Justin P Van BeusecumRalph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina, United States.ORCID 0000-0002-9265-9915
Edward W InschoDivision of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States.
Stephen KelleyDivision of Natural Sciences, University of Kent, Kent, United Kingdom.
Rebecca J LilleyDivision of Natural Sciences, University of Kent, Kent, United Kingdom.ORCID 0000-0002-9944-5944
Anthony K CookDivision of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, United States.
Kirsti D TaylorDivision of Natural Sciences, University of Kent, Kent, United Kingdom.ORCID 0000-0003-4379-1095
Claire M Peppiatt-WildmanDivision of Natural Sciences, University of Kent, Kent, United Kingdom.ORCID 0000-0002-4406-8571
Medway School of Pharmacy · GBUniversity of Alabama at Birmingham · USMedical University of South Carolina · US

Funding

TLR4 in the Regulation of Renal Microvascular FunctionR01DK044628 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI INSCHO, EDWARD W · 2000 to 2021
$6.2M
The Inflammatory Cytokines, MCP-1 and TGF-Beta, Mediate Renal Autoregulatory ImpaR01HL098135 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI INSCHO, EDWARD W · 2010 to 2014
$1.8M
A Role of GAS6/Axl Signaling in the Development of Essential HypertensionIK2BX005605 · VA · VETERANS HEALTH ADMINISTRATION · PI VAN BEUSECUM, JUSTIN PIETER · 2021 to 2025
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PURINERGIC REGULATION OF THE RENAL MICROVASCULATURER29DK044628 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI INSCHO, EDWARD W. · 1994 to 1998
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BLRD VA IK2 BX005605NHLBI NIH HHS R01 HL098135NIDDK NIH HHS R01 DK044628NIDDK NIH HHS R29 DK044628
6 · The paper itself

Abstract

The presence of a renal GABA/glutamate system has previously been described; however, its functional significance in the kidney remains undefined. We hypothesized, given its extensive presence in the kidney, that activation of this GABA/glutamate system would elicit a vasoactive response from the renal microvessels. The functional data here demonstrate, for the first time, that activation of endogenous GABA and glutamate receptors in the kidney significantly alters microvessel diameter with important implications for influencing renal blood flow. Renal blood flow is regulated in both the renal cortical and medullary microcirculatory beds via diverse signaling pathways. GABA- and glutamate-mediated effects on renal capillaries are strikingly similar to those central to the regulation of central nervous system capillaries, that is, exposing renal tissue to physiological concentrations of GABA, glutamate, and glycine led to alterations in the way that contractile cells, pericytes, and smooth muscle cells, regulate microvessel diameter in the kidney. Since dysregulated renal blood flow is linked to chronic renal disease, alterations in the renal GABA/glutamate system, possibly through prescription drugs, could significantly impact long-term kidney function.

Indexed as

Glutamic AcidGlycineCentral Nervous Systemgamma-Aminobutyric AcidKidneyMicrocirculationNeurotransmitter Agentsgamma-Aminobutyric AcidGlutamic AcidGlycineNeurotransmitter Agentsafferent arteriolehemodynamicsmicrovascular functionpericytesrenal blood flow

Identifiers

PMID37102686
PMCPMC10511176
OpenAlexW4367175011

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.