CoChat
Sign Up
Cited by 313Nitric Oxide and Endothelin EffectsCardiovascular Health and Disease PreventionEicosanoids and Hypertension Pharmacology

The DOI matches its Crossref record; 78 of the 79 references it cites were found in a registry or an index.

Endothelium-derived nitric oxide and vascular physiology and pathology

Open access
Arnal, J.-F., Dinh-Xuan, A.-T., Pueyo, M., Darblade, B., Rami, J.·1999·Cellular and Molecular Life Sciences
DOI 10.1007/s000180050358PMC PMC11146781
Open this paper in CoChat — free account

Abstract

In 1980, Furchgott and Zawadzki demonstrated that the relaxation of vascular smooth muscle cells in response to acetylcholine is dependent on the anatomical integrity of the endothelium. Endothelium-derived relaxing factor was identified 7 years later as the free radical gas nitric oxide (NO). In endothelium, the amino acid L-arginine is converted to L-citrulline and NO by one of the three NO synthases, the endothelial isoform (eNOS). Shear stress and cell proliferation appear to be, quantitatively, the two major regulatory factors of eNOS gene expression. However, eNOS seems to be mainly regulated by modulation of its activity. Stimulation of specific receptors to various agonists (e.g., bradykinin, serotonin, adenosine, ADP/ATP, histamine, thrombin) increases eNOS enzymatic activity at least in part through an increase in intracellular free Ca2+. However, the mechanical stimulus shear stress appears again to be the major stimulus of eNOS activity, although the precise mechanisms activating the enzyme remain to be elucidated. Phosphorylation and subcellular translocation (from plasmalemmal caveolae to the cytoskeleton or cytosol) are probably involved in these regulations. Although eNOS plays a major vasodilatory role in the control of vasomotion, it has not so far been demonstrated that a defect in endothelial NO production could be responsible for high blood pressure in humans. In contrast, a defect in endothelium-dependent vasodilation is known to be promoted by several risk factors (e.g., smoking, diabetes, hypercholesterolemia) and is also the consequence of atheroma (fatty streak infiltration of the neointima). Several mechanisms probably contribute to this decrease in NO bioavailability. Finally, a defect in NO generation contributes to the pathophysiology of pulmonary hypertension. Elucidation of the mechanisms of eNOS enzyme activity and NO bioavailability will contribute to our understanding the physiology of vasomotion and the pathophysiology of endothelial dysfunction, and could provide insights for new therapies, particularly in hypertension and atherosclerosis.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1007/s000180050358

Cites

78 of 78 references verified0 citation errors · 0 not checkable

Statistics

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 79 references

Research works printed but not linked: 1

  1. 60 White C. R., Brock T. A., Chang L. Y., Crapo J., Briscoe P., Ku D. et al. (1994) Superoxide and peroxynitrite in atherosclerosis. Proc. Natl. Acad. Sci. USA 91: 1044-1048

Cited by

Sorted by citations

Items 201–300 of 313

Related

See all

Metadata

Authors
Arnal, J.-F., Dinh-Xuan, A.-T., Pueyo, M., Darblade, B., & Rami, J.
Affiliations
Inserm (FR)
ORCID
Arnal, J.-F.
Venue
Cellular and Molecular Life Sciences
Publisher
Springer Science and Business Media LLC
Published
1999
Volume
55
Issue
9
Pages
1078
ISSN
1420-682X (ISSN-L)
DOI
10.1007/s000180050358
PMC
PMC11146781
OpenAlex
W2093217834
Cited by
313
References
79
Citations by year
2026: 3 · 2025: 7 · 2024: 6 · 2023: 6 · 2022: 4 · 2021: 1 · 2020: 5 · 2019: 12 · 2018: 4 · 2017: 9 · 2016: 10 · 2015: 16 · 2014: 13 · 2013: 8 · 2012: 15
FWCI
6.04
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Cellular and Molecular Life Sciences (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Health and Disease Prevention
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Eicosanoids and Hypertension Pharmacology
Keywords
nitric oxide, endothelium-derived relaxing factor, endothelial nitric oxide synthase, shear stress, endothelial dysfunction, NO bioavailability, endothelium-dependent vasodilation, vasomotion, hypertension, atherosclerosis, pulmonary hypertension, L-arginine, intracellular calcium, eNOS phosphorylation, subcellular translocation
MeSH terms
Animals, Arginine, Arteriosclerosis, Blood Vessels, Cell Adhesion, Endothelium, Vascular, Enzyme Induction, Enzyme Inhibitors, Humans, Hypertension, Hypertension, Pulmonary, Isoenzymes, Membrane Proteins, Nitric Oxide, Rabbits, Vascular Diseases, Vasodilation, Signal Transduction, Oxidative Stress, Nitric Oxide Synthase, omega-N-Methylarginine, NG-Nitroarginine Methyl Ester, Caveolins, Caveolin 1, Nitric Oxide Synthase Type III

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review