Evidence map›Paper›PMID 37058193›Full record

ReviewCurrent hypertension reports2023

Neurogenic Background for Emotional Stress-Associated Hypertension.

Marco Antônio Peliky Fontes, Fernanda Ribeiro Marins, Tapan A Patel, Cristiane Amorim de Paula, Liliane Ramos Dos Santos Machado, Érick Bryan de Sousa Lima, Ana Caroline Ventris-Godoy, Ana Clara Rocha Viana, Isadora Cristina Souza Linhares, Carlos Henrique Xavier and 2 more

Open access · bronzeAbstract readReview
In one paragraph

Review in Current hypertension reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
8.6field-weighted citation impact, top 2% 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

29 citing papers in PubMed, 39 citations in OpenAlex.

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  20. Management of obesity in an individual with ROHHAD syndrome with semaglutide 2.4 mg/week: a case report.Clinical autonomic research : official journal of the Clinical Autonomic Research Society · 2025
    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

12 authors at 4 institutions in 2 countries.

Marco Antônio Peliky FontesDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil. peliky@icb.ufmg.br.ORCID 0000-0003-4525-3565
Fernanda Ribeiro MarinsDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Tapan A PatelDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE, USA.
Cristiane Amorim de PaulaDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Liliane Ramos Dos Santos MachadoDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Érick Bryan de Sousa LimaDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Ana Caroline Ventris-GodoyDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Ana Clara Rocha VianaDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Isadora Cristina Souza LinharesDepartment of Physiology & Biophysics, Federal University of Minas Gerais, Federal de Minas Gerais, Belo Horizonte, MG, 31270 901, Brazil.
Carlos Henrique XavierInstitute of Biological Sciences, Federal University of Goias, Goiania, Brazil.
Jessica A FilosaDepartment of Physiology, Augusta University, Augusta, GA, USA.
Kaushik P PatelDepartment of Cellular and Integrative Physiology, University of Nebraska Medical Center, Omaha, NE, USA.
Universidade Federal de Minas Gerais · BRUniversity of Nebraska Medical Center · USAugusta University · USUniversidade Federal de Goiás · BR

Funding

Novel Target Mechanism (Renal Denervation) to Reduce Sodium Retention in Chronic Heart FailureR01DK114663 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PATEL, KAUSHIK P, ZHENG, HONG · 2017 to 2021
$2.1M
Novel target mechanism (renal nerves) for the beneficial actions of SGLT2 inhibition in congestive heart failureR01DK129311 · NIDDK · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI PATEL, KAUSHIK P, ZHENG, HONG · 2021 to 2024
$2.0M
Clinically unscreened vasculo-glial-neuronal coupling is critical for physiological brain functionR01NS097818 · NINDS · AUGUSTA UNIVERSITY · PI FILOSA, JESSICA A · 2017 to 2021
$1.8M
NIDDK NIH HHS R01 DK114663NIDDK NIH HHS R01 DK129311NINDS NIH HHS R01 NS097818
6 · The paper itself

Abstract

purpose of reviewThe response to natural stressors involves both cardiac stimulation and vascular changes, primarily triggered by increases in sympathetic activity. These effects lead to immediate flow redistribution that provides metabolic support to priority target organs combined with other key physiological responses and cognitive strategies, against stressor challenges. This extremely well-orchestrated response that was developed over millions of years of evolution is presently being challenged, over a short period of time. In this short review, we discuss the neurogenic background for the origin of emotional stress-induced hypertension, focusing on sympathetic pathways from related findings in humans and animals. RECENT

findingsThe urban environment offers a variety of psychological stressors. Real or anticipatory, emotional stressors may increase baseline sympathetic activity. From routine day-to-day traffic stress to job-related anxiety, chronic or abnormal increases in sympathetic activity caused by emotional stressors can lead to cardiovascular events, including cardiac arrhythmias, increases in blood pressure and even sudden death. Among the various alterations proposed, chronic stress could modify neuroglial circuits or compromise antioxidant systems that may alter the responsiveness of neurons to stressful stimuli. These phenomena lead to increases in sympathetic activity, hypertension and consequent cardiovascular diseases. The link between anxiety, emotional stress, and hypertension may result from an altered neuronal firing rate in central pathways controlling sympathetic activity. The participation of neuroglial and oxidative mechanisms in altered neuronal function is primarily involved in enhanced sympathetic outflow. The significance of the insular cortex-dorsomedial hypothalamic pathway in the evolution of enhanced overall sympathetic outflow is discussed.

Indexed as

HypertensionPsychological DistressAnimalsBlood PressureHeartHumansHypothalamusSympathetic Nervous SystemAnxietyAutonomic nervous systemEmotional stressHypertensionSympathetic

Identifiers

PMID37058193
PMCPMC10103037
OpenAlexW4365478930

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.