Evidence mapPaperPMID 30129037Full record

ReviewBritish journal of pharmacology2019

The bidirectional interaction between the sympathetic nervous system and immune mechanisms in the pathogenesis of hypertension.

Revathy Carnagarin, Vance Matthews, Maria T K Zaldivia, Karlheinz Peter, Markus P Schlaich

Registry-linked trialAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04478500 (The Role of Neuroinflammation in Hypertension.Minocycline for Resistant Hypertension), which is not on this map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
field-weighted citation impact
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.

NCT04478500 phase3unknown statusnot on this mapstarted 2020, after this paper: background citation

The Role of Neuroinflammation in Hypertension.Minocycline for Resistant Hypertension: a Randomized Double Blind Placebo-Controlled Trial

TypeinterventionalSponsorRoyal Perth HospitalRan2020 to 2025Enrolled60ConditionsResistant HypertensionArmsMinocycline
3 · Its place in the literature

Who cites it

30 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  15. Risk Effects of rs1799945 Polymorphism of theInternational journal of molecular sciences · 2023
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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

5 authors.

Revathy CarnagarinDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, The University of Western Australia, Perth, WA, Australia.
Vance MatthewsDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, The University of Western Australia, Perth, WA, Australia.
Maria T K ZaldiviaAtherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute, Melbourne, Vic, Australia.
Karlheinz PeterAtherothrombosis and Vascular Biology, Baker Heart and Diabetes Institute, Melbourne, Vic, Australia.
Markus P SchlaichDobney Hypertension Centre, School of Medicine - Royal Perth Hospital Unit, The University of Western Australia, Perth, WA, Australia.ORCID 0000-0002-1765-0195

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Over the last few years, evidence has accumulated to suggest that hypertension is, at least in part, an immune-mediated inflammatory disorder. Many links between immunity and hypertension have been established and provide a complex framework of mechanistic interactions contributing to the rise in BP. These include immune-mediated inflammatory processes affecting regulatory brain nuclei and interactions with other mediators of cardiovascular regulation such as the sympathetic nervous system. Sympathoexcitation differentially regulates T-cells based upon activation status of the immune cell as well as the resident organ. Exogenous and endogenous triggers activate signalling pathways in innate and adaptive immune cells resulting in pro-inflammatory cytokine production and activation of T-lymphocytes in the cardiovascular and renal regions, now considered major factors in the development of essential hypertension. The inflammatory cascade is sustained and exacerbated by the immune flow via the brain-bone marrow-spleen-gastrointestinal axis and thereby further aggravating immune-mediated pathways resulting in a vicious cycle of established hypertension and target organ damage. This review summarizes the evidence and recent advances in linking immune-mediated inflammation, sympathetic activation and their bidirectional interactions with the development of hypertension. LINKED ARTICLES: This article is part of a themed section on Immune Targets in Hypertension. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v176.12/issuetoc.

Indexed as

AnimalsHumansHypertensionImmune System DiseasesInflammationSympathetic Nervous System

Identifiers

PMID30129037
PMCPMC6534787

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

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 Socratic graph.