Evidence map›Paper›PMID 15372104›Full record

ArticleThe Journal of clinical investigation2004

Decreased susceptibility to renovascular hypertension in mice lacking the prostaglandin I2 receptor IP.

Takayuki Fujino, Naoki Nakagawa, Koh-Ichi Yuhki, Akiyoshi Hara, Takehiro Yamada, Koji Takayama, Shuhko Kuriyama, Yayoi Hosoki, Osamu Takahata, Takanobu Taniguchi and 5 more

Abstract read
In one paragraph

Article in The Journal of clinical investigation, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
6.6field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 115 citations in OpenAlex.

  1. Prostaglandin EHeart and vessels · 2023
    Article
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Regulation of renin release via cyclic ADP-ribose-mediated signaling: evidence from mice lacking CD38 gene.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2013
    Article
  15. Physiologic and pathophysiologic roles of cyclooxygenase-2 in the kidney.Transactions of the American Clinical and Climatological Association · 2013
    Article
  16. Eplerenone inhibits aldosterone-induced renal expression of cyclooxygenase.Journal of the renin-angiotensin-aldosterone system : JRAAS · 2012
    Article
  17. Review
  18. Review
  19. Article
  20. A major role for the EP4 receptor in regulation of renin.American journal of physiology. Renal physiology · 2011
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 2 institutions in 1 country.

Takayuki FujinoDepartment of Pharmacology, Asahikawa Medical College, Japan.
Naoki Nakagawa
Koh-Ichi Yuhki
Akiyoshi Hara
Takehiro Yamada
Koji Takayama
Shuhko Kuriyama
Yayoi Hosoki
Osamu Takahata
Takanobu Taniguchi
Jun Fukuzawa
Naoyuki Hasebe
Kenjiro Kikuchi
Shuh Narumiya
Fumitaka Ushikubi
Asahikawa Medical University · JPAsahikawa Medical College Hospital · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Persistent reduction of renal perfusion pressure induces renovascular hypertension by activating the renin-angiotensin-aldosterone system; however, the sensing mechanism remains elusive. Here we investigated the role of PGI2 in renovascular hypertension in vivo, employing mice lacking the PGI2 receptor (IP-/- mice). In WT mice with a two-kidney, one-clip model of renovascular hypertension, the BP was significantly elevated. The increase in BP in IP-/- mice, however, was significantly lower than that in WT mice. Similarly, the increases in plasma renin activity, renal renin mRNA, and plasma aldosterone in response to renal artery stenosis were all significantly lower in IP-/- mice than in WT mice. All these parameters were measured in mice lacking the four PGE2 receptor subtypes individually, and we found that these mice had similar responses to WT mice. PGI2 is produced by COX-2 and a selective inhibitor of this enzyme, SC-58125, also significantly reduced the increases in plasma renin activity and renin mRNA expression in WT mice with renal artery stenosis, but these effects were absent in IP-/- mice. When the renin-angiotensin-aldosterone system was activated by salt depletion, SC-58125 blunted the response in WT mice but not in IP-/- mice. These results indicate that PGI2 derived from COX-2 plays a critical role in regulating the release of renin and consequently renovascular hypertension in vivo.

Indexed as

AnimalsBlood PressureCreatinineCrosses, GeneticCyclooxygenase InhibitorsDinoprostoneEpoprostenolGene Expression RegulationGenetic Predisposition to DiseaseHypertension, RenalInfarctionMiceMice, Inbred C57BLMice, KnockoutNephrectomyProstaglandin-Endoperoxide Synthases1-((4-methylsulfonyl)phenyl)-3-trifluoromethyl-5-(4-fluorophenyl)pyrazoleCreatinineCyclooxygenase InhibitorsDinoprostoneEpoprostenolProstaglandin-Endoperoxide SynthasesPyrazolesReceptors, EpoprostenolRNA, Messenger

Identifiers

PMID15372104
PMCPMC516260
OpenAlexW2160684878

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.