Evidence map›Paper›PMID 22458740›Full record

ReviewJournal of clinical hypertension (Greenwich, Conn.)2012

Impaired vasodilation in the pathogenesis of hypertension: focus on nitric oxide, endothelial-derived hyperpolarizing factors, and prostaglandins.

Thomas D Giles, Gary E Sander, Bobby D Nossaman, Philip J Kadowitz

Registry-linked trialOpen access · bronzeAbstract readReview
In one paragraph

Review in Journal of clinical hypertension (Greenwich, Conn.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04993664 (Influence of Pelacarsen on Arterial Wall Properties and Risk Factors in Patients After Myocardial Infarction With High Lp), which is not on this map. Cited by 87 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% 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.

NCT04993664 nawithdrawnnot on this mapstarted 2021, after this paper: background citation

Influence of Pelacarsen on Arterial Wall Properties and Risk Factors in Patients After Myocardial Infarction With High Lp(a) Values

TypeinterventionalSponsorUniversity Medical Centre LjubljanaRan2021 to 2022Enrolled0ConditionsAcute Coronary Syndrome, Lipoproteinemia, Inflammation, Genetic PolymorphismsArmsPelacarsen (TQJ230), Placebo
3 · Its place in the literature

Who cites it

87 citing papers in PubMed, 1 synthesis or guideline pooled it, 190 citations in OpenAlex.

  1. Pooled it
  2. Unravelling the Therapeutic Potential of Cysteine for Cardiovascular Health.International journal of molecular sciences · 2026
    Review
  3. Biomedical optics express · 2026
    Article
  4. Article
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  14. Racial Physiology: A Dangerous Precedent.American journal of respiratory and critical care medicine · 2024
    Article
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  16. Review
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27 more citing papers are in PubMed but not listed here.

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

4 authors at 3 institutions in 1 country.

Thomas D GilesHeart & Vascular Institute, Tulane University Medical Center, New Orleans, LA, USA. tgiles4@cox.net
Gary E Sander
Bobby D Nossaman
Philip J Kadowitz
Tulane Medical Center · USTulane University · USUniversity Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Under resting conditions the arterial vasculature exists in a vasoconstricted state referred to as vascular tone. Physiological dilatation in response to increased flow, a function of normal endothelium is necessary to maintain normal blood pressure. Endothelial dysfunction in vascular smooth muscle cells thus results in loss of normal vasorelaxant function and the inability of arteries to appropriately dilate in response to increased blood flow in either a systemic or regional vascular bed, resulting in increased blood pressure, a sequence that may represent a common pathway to hypertension. Normal vasorelaxation is mediated by a number of endothelial systems including nitric oxide (NO), prostaglandins (PGI2 and PGE2), and a family of endothelial-derived hyperpolarizing factors (EDHF). In response to hemodynamic shear stress, endothelium continuously releases NO, EDHF, and PGI2 to provide vasodilatation. EDHF, not a single molecule but rather a group of molecules that includes epoxyeicosatrienoic acids, hydrogen peroxide, carbon monoxide, hydrogen sulfide, C-natriuretic peptide, and K+ itself, causes vasodilatation by activation of vascular smooth muscle cell K+ channels, resulting in hyperpolarization and thus vasorelaxation. The understanding and effective management of blood pressure requires an understanding of both physiologic and pathophysiologic regulation of vascular tone. This review describes molecular mechanisms underlying normal endothelial regulation and pathological states, such as increased oxidative stress, which cause loss of vasorelaxation. Possible pharmacological interventions to restore normal function are suggested.

Indexed as

Biological FactorsEndothelinsEndothelium, VascularHumansHypertensionNitric OxideOxidative StressPotassium ChannelsProstaglandinsVasodilationBiological FactorsEndothelinsendothelium-dependent hyperpolarization factorNitric OxidePotassium ChannelsProstaglandins

Identifiers

PMID22458740
PMCPMC8108814
OpenAlexW1643585163

What OpenQuestion 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 OpenQuestion graph.