Evidence map›Paper›PMID 15837925›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

The rapid release of corticosterone from the adrenal induced by ACTH is mediated by nitric oxide acting by prostaglandin E2.

Claudia E Mohn, Javier Fernandez-Solari, Andrea De Laurentiis, Juan Pablo Prestifilippo, Carolina de la Cal, Richard Funk, Stefan R Bornstein, Samuel M McCann, Valeria Rettori

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.5field-weighted citation impact, top 22% 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

24 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Thromboxane AAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  5. Review
  6. Eicosanoids: Atherosclerosis and cardiometabolic health.Journal of clinical & translational endocrinology · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Time-dependent mediators of HPA axis activation following live Escherichia coli.American journal of physiology. Regulatory, integrative and comparative physiology · 2011
    Article
  18. Article
  19. 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

9 authors at 2 institutions in 1 country.

Claudia E MohnCentro de Estudios Farmacológicos y Botánicos, Consejo Nacional de Investigaciones Científicas y Técnicas, Serrano 669, 1414 Buenos Aires, Argentina.
Javier Fernandez-Solari
Andrea De Laurentiis
Juan Pablo Prestifilippo
Carolina de la Cal
Richard Funk
Stefan R Bornstein
Samuel M McCann
Valeria Rettori
Consejo Nacional de Investigaciones Científicas y Técnicas · ARUniversity of Buenos Aires · AR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adrenal cortex is a major stress organ in mammals that reacts rapidly to a multitude of external and internal stressors. Adrenocorticotropin (ACTH) is the main stimulator of the adrenal cortex, activating corticosteroid synthesis and secretion. We evaluated the mechanism of action of ACTH on adrenals of male rats, preserving the architecture of the gland in vitro. We demonstrated that both sodium nitroprusside (NP), a nitric oxide (NO) donor, and ACTH stimulate corticosterone release. NO mediated the acute response to ACTH because Nomega-nitro-l-arginine methyl ester, a NO synthase inhibitor, and hemoglobin, a NO scavenger, blocked the stimulation of corticosterone release induced by ACTH. NP stimulated prostaglandin E release, which in turn stimulated corticosterone release from the adrenal. Additionally, indomethacin, which inhibits cyclooxygenase, and thereby, prostaglandin release, prevented corticosterone release from the adrenal induced by both NP and ACTH, demonstrating that prostaglandins mediate acute corticosterone release. Corticosterone content in adrenals after incubation with ACTH or NP was lower than in control glands, indicating that any de novo synthesis of corticosterone during this period was not sufficient to keep up with the release of the stored hormone. The release induced by ACTH or NP depleted the corticosterone content in the adrenal by approximately 40% compared with the content of glands incubated in buffer. The mechanism of rapid release is as follows: NO produced by NO synthase activation by ACTH activates cyclooxygenase, which generates PGE(2), which in turn releases corticosterone stored in microvesicles and other organelles.

Indexed as

Adrenal CortexAdrenocorticotropic HormoneAnimalsCorticosteroneDinoprostoneMaleNG-Nitroarginine Methyl EsterNitric OxideNitroprussideRatsRats, WistarAdrenocorticotropic HormoneCorticosteroneDinoprostoneNG-Nitroarginine Methyl EsterNitric OxideNitroprusside

Identifiers

PMID15837925
PMCPMC1087960
OpenAlexW2000264966

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.