Evidence map›Paper›PMID 12379820›Full record

ReviewHeart failure reviews2002

Angiotensin II and nitric oxide interaction.

Marc de Gasparo

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 78 citations in OpenAlex.

  1. Trial
  2. Characterization of a robust mouse model of heart failure with preserved ejection fraction.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  3. Review
  4. Article
  5. Review
  6. Article
  7. Insights in Chloroquine Action: Perspectives and Implications in Malaria and COVID-19.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2020
    Review
  8. Article
  9. Effects of Local Pancreatic Renin-Angiotensin System on the Microcirculation of Rat with Severe Acute Pancreatitis.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2015
    Article
  10. Article
  11. Review
  12. Review
  13. Morphine and angiogenesis in hypertensive animals.Iranian journal of basic medical sciences · 2012
    Article
  14. Local renin-angiotensin systems in the genitourinary tract.Naunyn-Schmiedeberg's archives of pharmacology · 2012
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  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

1 author.

Marc de GasparoMG Consulting Co, Rossemaison, Switzerland. m.de_gasparo@bluewin.ch

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide degradation linked to endothelial dysfunction plays a central role in cardiovascular diseases. Superoxide producing enzymes such as NADPH oxidase and xanthine oxidase are responsible for NO degradation as they generate a variety of reactive oxygen species (ROS). Moreover, superoxide is rapidly degraded by superoxide dismutase to produce hydrogen peroxide leading to the uncoupling of NO synthase and production of increased amount of superoxide. Angiotensin II is an important stimulus of NADPH oxidase. Through its AT(1) receptor, Ang II stimulates the long-term increase of several membrane component of NADPH oxidase such as P(22) phox or nox-1 and causes an increased activity of NADPH oxidase with inactivation of NO leading to impaired endothelium-dependent vasorelaxation, vascular smooth muscle cell hypertrophy, proliferation and migration, extracellular matrix formation, thrombosis, cellular infiltration and inflammatory reaction. Several preclinical and clinical studies have now confirmed the involvement of the AT(1) receptor in endothelial dysfunction. It is proposed that the AT(2) receptor counterbalances the deleterious effect of the Ang II-induced AT(1) receptor stimulation through bradykinin and NOS stimulation. This mechanism could be especially relevant in pathological cases when the NADPH oxidase activity is blocked with an AT(1) receptor antagonist.

Indexed as

Angiotensin IIEndothelium, VascularHumansNADH, NADPH OxidoreductasesNitric OxideReactive Oxygen SpeciesReceptors, AngiotensinAngiotensin IINADH, NADPH OxidoreductasesNitric OxideReactive Oxygen SpeciesReceptors, Angiotensin

Identifiers

PMID12379820
OpenAlexW1518058648

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.