Evidence map›Paper›PMID 30332305›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2018

Pharmacological potentiation of the efferent vagus nerve attenuates blood pressure and renal injury in a murine model of systemic lupus erythematosus.

Grace S Pham, Lei A Wang, Keisa W Mathis

Open access · bronzeAbstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

28 citing papers in PubMed, 33 citations in OpenAlex.

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  10. Electrical neuromodulation therapy for inflammatory bowel disease.World journal of gastrointestinal pathophysiology · 2022
    Review
  11. Review
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  13. Article
  14. Autoimmune-mediated renal disease and hypertension.Clinical science (London, England : 1979) · 2021
    Review
  15. Review
  16. Review
  17. Autonomic and cholinergic mechanisms mediating cardiovascular and temperature effects of donepezil in conscious mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2021
    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

3 authors at 1 institution in 1 country.

Grace S PhamDepartment of Physiology and Anatomy, University of North Texas Health Science Center , Fort Worth, Texas.
Lei A WangDepartment of Physiology and Anatomy, University of North Texas Health Science Center , Fort Worth, Texas.ORCID 0000-0003-3549-4306
Keisa W MathisDepartment of Physiology and Anatomy, University of North Texas Health Science Center , Fort Worth, Texas.
University of North Texas · US

Funding

Neuroimmune Mechanisms Involved in the Pathogenesis of Hypertension and Renal InjuryK01HL139859 · NHLBI · UNIVERSITY OF NORTH TEXAS HLTH SCI CTR · PI MATHIS, KEISA WILLIAMS · 2018 to 2022
$770k
NHLBI NIH HHS K01 HL139859
6 · The paper itself

Abstract

Recent evidence suggests hypertension may be secondary to chronic inflammation that results from hypoactive neuro-immune regulatory mechanisms. To further understand this association, we used systemic lupus erythematosus (SLE) as a model of inflammation-induced hypertension. In addition to prevalent inflammatory kidney disease and hypertension, SLE patients suffer from dysautonomia in the form of decreased efferent vagal tone. Based on this, the cholinergic anti-inflammatory pathway, an endogenous vagus-to-spleen mechanism that, when activated results in decreases in systemic inflammation, may be compromised in SLE. We hypothesized that stimulation of the cholinergic anti-inflammatory pathway via pharmacological potentiation of the efferent vagus nerve would reduce inflammation and halt the development of hypertension and renal injury in SLE. Female NZBWF1 mice, an established model of murine SLE, and female control mice were treated with galantamine (4 mg/kg daily ip), an acetylcholinesterase inhibitor, or saline for 14 days. At the end of therapy, carotid catheters were surgically implanted and were used to measure mean arterial pressure before the animals were euthanized. Chronic galantamine administration attenuated both splenic and renal cortical inflammation, which likely explains why the hypertension and renal injury (i.e., glomerulosclerosis and fibrosis) typically observed in murine SLE was attenuated following therapy. Based on this, the anti-inflammatory, antihypertensive, and renoprotective effects of galantamine may be mediated through activation of the cholinergic anti-inflammatory pathway. It is possible that dysfunction of the cholinergic anti-inflammatory pathway exists in SLE at the level of the efferent vagus nerve and promoting restoration of its activity through central cholinergic receptor activation may be beneficial.

Indexed as

AnimalsAntihypertensive AgentsBlood PressureCholinesterase InhibitorsDisease Models, AnimalGalantamineHypertensionKidneyMice, TransgenicNeurons, EfferentVagus NerveAntihypertensive AgentsCholinesterase InhibitorsGalantaminegalantaminehypertensionlupus nephritisneuroimmunerenal inflammation

Identifiers

PMID30332305
PMCPMC6425635
OpenAlexW2897909832

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.