Evidence map›Paper›PMID 25857326›Full record

ReviewJournal of clinical hypertension (Greenwich, Conn.)2015

Endothelial Function in Hypertension: Victim or Culprit?

Caroline Bleakley, Paul Kevin Hamilton, Richard Pumb, Mark Harbinson, Gary Eugene McVeigh

Abstract readReview
In one paragraph

Review in Journal of clinical hypertension (Greenwich, Conn.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
–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.

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

25 citing papers in PubMed.

  1. Trial
  2. Review
  3. A mechanistic study on the enhanced antihypertensive effects of aFrontiers in cell and developmental biology · 2026
    Article
  4. Review
  5. Article
  6. Pulse Pressure Impairs Cognition via White Matter Disruption.Hypertension (Dallas, Tex. : 1979) · 2025
    Article
  7. Natural Products to Promote Vascular Health.Handbook of experimental pharmacology · 2025
    Review
  8. Article
  9. Associations for progression of cerebral small vessel disease burden in healthy adults: the Kashima scan study.Hypertension research : official journal of the Japanese Society of Hypertension · 2024
    Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Acute e-cig inhalation impacts vascular health: a study in smoking naïve subjects.American journal of physiology. Heart and circulatory physiology · 2021
    Article
  15. TRPC and TRPV Channels' Role in Vascular Remodeling and Disease.International journal of molecular sciences · 2020
    Review
  16. Review
  17. Review
  18. Review
  19. Article
  20. Review
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.

Caroline BleakleyDepartment of Cardiovascular Therapeutics & Pharmacology, Queen's University Belfast, Belfast, UK.
Paul Kevin HamiltonDepartment of Cardiovascular Therapeutics & Pharmacology, Queen's University Belfast, Belfast, UK.
Richard PumbDepartment of Cardiovascular Therapeutics & Pharmacology, Queen's University Belfast, Belfast, UK.
Mark HarbinsonDepartment of Cardiovascular Therapeutics & Pharmacology, Queen's University Belfast, Belfast, UK.
Gary Eugene McVeighDepartment of Cardiovascular Therapeutics & Pharmacology, Queen's University Belfast, Belfast, UK.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Far from simply lining the inner surface of blood vessels, the cellular monolayer that comprises the endothelium is a highly active organ that regulates vascular tone. In health, the endothelium maintains the balance between opposing dilator and constrictor influences, while in disease, it is the common ground on which cardiovascular risk factors act to initiate the atherosclerotic process. As such, it is the site at which cardiovascular disease begins and consequently acts as a barometer of an individual's likely future cardiovascular health. The vascular endothelium is a very active organ responsible for the regulation of vascular tone through the effects of locally synthesized mediators, predominantly nitric oxide (NO), endothelial NO synthase (eNOS), and superoxide. NO is abundantly evident in normally functioning vasculature where it acts as a vasodilator, inhibits inflammation, and has an antiaggregant effect on platelets. Its depletion is both a sign and cause of endothelial dysfunction resulting from reduced activity of eNOS and amplified production of nicotinamide adenine dinucleotide oxidase, which, in turn, results in raised levels of reactive oxygen species. This cascade is the basis for reduced vascular compliance through an imbalanced regulation of tone with a predominance of vasoconstrictive elements. Further, structural changes in the microvasculature are a critical early step in the loss of normal function. This microvascular dysfunction is known to be highly predictive of future macrovascular events and is consequently a very attractive target for intervention in the hypertensive population in order to prevent cardiovascular events.

Indexed as

Cardiovascular DiseasesEndothelium, VascularHumansHypertensionNitric OxideNitric Oxide Synthase Type IIIReactive Oxygen SpeciesRisk FactorsNitric OxideNitric Oxide Synthase Type IIIReactive Oxygen Species

Identifiers

PMID25857326
PMCPMC8031772

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.