Evidence map›Paper›PMID 26290101›Full record

ReviewAmerican journal of physiology. Regulatory, integrative and comparative physiology2015

The roles of sensitization and neuroplasticity in the long-term regulation of blood pressure and hypertension.

Alan Kim Johnson, Zhongming Zhang, Sarah C Clayton, Terry G Beltz, Seth W Hurley, Robert L Thunhorst, Baojian Xue

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Regulatory, integrative and comparative physiology, 2015. 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
2.8field-weighted citation impact, top 9% 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, 54 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. When Memory Does Not Serve You Well.Circulation research · 2020
    Article
  12. Amphetamine-induced sensitization of hypertension and lamina terminalis neuroinflammation.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. ATAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2019
    Article
  18. Review
  19. ATAmerican journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  20. 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

7 authors at 2 institutions in 2 countries.

Alan Kim JohnsonDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa; Department of Health and Human Physiology, The University of Iowa, Iowa City, Iowa; Department of Pharmacology, The University of Iowa, Iowa City, Iowa; François M. Abboud Cardiovascular Center, The University of Iowa, Iowa City, Iowa; and alan-johnson@uiowa.edu.
Zhongming ZhangDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa; Nanyang Institute of Technology, Zhang Zhongjing College of Chinese Medicine, Nanyang, Henan Province, China.
Sarah C ClaytonDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa;
Terry G BeltzDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa;
Seth W HurleyDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa;
Robert L ThunhorstDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa; François M. Abboud Cardiovascular Center, The University of Iowa, Iowa City, Iowa; and.
Baojian XueDepartment of Psychological and Brain Sciences, The University of Iowa, Iowa City, Iowa; François M. Abboud Cardiovascular Center, The University of Iowa, Iowa City, Iowa; and.
University of Iowa · USNanyang Institute of Technology · CN

Funding

VASOPRESSIN IN CARDIOVASCULAR REGULATIONP01HL014388 · NHLBI · UNIVERSITY OF IOWA · PI ABBOUD, FRANCOIS M · 1985 to 2018
$40.3M
Thirst Deficits in Rat Model of AgingR01AG025465 · NIA · UNIVERSITY OF IOWA · PI THUNHORST, ROBERT L · 2005 to 2015
$2.4M
The Stress of Chronic Disease: Mineralocorticoid Mediation of MoodR01MH080241 · NIMH · UNIVERSITY OF IOWA · PI JOHNSON, ALAN KIM · 2010 to 2014
$1.7M
Neural Control of the Circulation: Sex and HypertensionR01HL098207 · NHLBI · UNIVERSITY OF IOWA · PI JOHNSON, ALAN KIM, XUE, BAOJIAN · 2010 to 2013
$1.5M
NHLBI NIH HHS HL-098207NHLBI NIH HHS HL-14388NHLBI NIH HHS P01 HL014388NHLBI NIH HHS R01 HL098207NIA NIH HHS R01 AG025465NIMH NIH HHS MH-08241NIMH NIH HHS R01 MH080241
6 · The paper itself

Abstract

After decades of investigation, the causes of essential hypertension remain obscure. The contribution of the nervous system has been excluded by some on the basis that baroreceptor mechanisms maintain blood pressure only over the short term. However, this point of view ignores one of the most powerful contributions of the brain in maintaining biological fitness-specifically, the ability to promote adaptation of behavioral and physiological responses to cope with new challenges and maintain this new capacity through processes involving neuroplasticity. We present a body of recent findings demonstrating that prior, short-term challenges can induce persistent changes in the central nervous system to result in an enhanced blood pressure response to hypertension-eliciting stimuli. This sensitized hypertensinogenic state is maintained in the absence of the inducing stimuli, and it is accompanied by sustained upregulation of components of the brain renin-angiotensin-aldosterone system and other molecular changes recognized to be associated with central nervous system neuroplasticity. Although the heritability of hypertension is high, it is becoming increasingly clear that factors beyond just genes contribute to the etiology of this disease. Life experiences and attendant changes in cellular and molecular components in the neural network controlling sympathetic tone can enhance the hypertensive response to recurrent, sustained, or new stressors. Although the epigenetic mechanisms that allow the brain to be reprogrammed in the face of challenges to cardiovascular homeostasis can be adaptive, this capacity can also be maladaptive under conditions present in different evolutionary eras or ontogenetic periods.

Indexed as

Blood PressureNeuronal PlasticityAdaptation, PhysiologicalAldosteroneAngiotensin IIAnimalsCardiovascular SystemCentral Nervous SystemDisease Models, AnimalGenetic Predisposition to DiseaseHeredityHumansHypertensionRenin-Angiotensin SystemRisk FactorsSignal TransductionAldosteroneAngiotensin IIaldosteronecross-sensitizationinduction-delay-expression paradigmneural networks controlling blood pressurerenin-angiotensin-aldosterone systemssalt sensitivityslow pressor angiotensin-elicited hypertension

Identifiers

PMID26290101
PMCPMC4698407
OpenAlexW2269532196

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.