Evidence map›Paper›PMID 12874088›Full record

ArticleHypertension (Dallas, Tex. : 1979)2003

Role of angiotensin II and reactive oxygen species in cyclosporine A-dependent hypertension.

Akira Nishiyama, Hiroyuki Kobori, Toshiki Fukui, Guo-Xing Zhang, Li Yao, Matlubur Rahman, Hirofumi Hitomi, Hideyasu Kiyomoto, Takatomi Shokoji, Shoji Kimura and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
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  5. Review
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  7. Article
  8. Calcineurin dephosphorylates Kelch-like 3, reversing phosphorylation by angiotensin II and regulating renal electrolyte handling.Proceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Central modulation of cyclosporine-induced hypertension.Naunyn-Schmiedeberg's archives of pharmacology · 2015
    Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. The role of Toll-like receptors in renal diseases.Nature reviews. Nephrology · 2010
    Review
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

12 authors at 1 institution in 2 countries.

Akira NishiyamaDepartment of Pharmacology, Kagawa Medical University, 1750-1 Ikenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan. akira@kms.ac.jp
Hiroyuki Kobori
Toshiki Fukui
Guo-Xing Zhang
Li Yao
Matlubur Rahman
Hirofumi Hitomi
Hideyasu Kiyomoto
Takatomi Shokoji
Shoji Kimura
Masakazu Kohno
Youichi Abe
Tulane University · US

Funding

Intrarenal Augmentation of Angiotensinogen by Ang IIR01DK072408 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2006 to 2010
$1.2M
NIDDK NIH HHS R01 DK072408
6 · The paper itself

Abstract

Treatment with cyclosporine A (CysA), a potent immunosuppressive agent, is associated with systemic and renal vasoconstriction, leading to hypertension. The present study was conducted to elucidate the contribution of angiotensin II (Ang II) to CysA-induced hypertension and reactive oxygen species (ROS) generation. CysA (30 mg/kg per day SC), given for 3 weeks in rats, increased systolic blood pressure (SBP) from 119+/-2 to 145+/-3 mm Hg (n=7). Plasma and kidney Ang II levels were significantly higher in CysA-treated rats (136+/-10 fmol/mL and 516+/-70 fmol/g) than in vehicle-treated (1 mL olive oil) rats (76+/-10 fmol/mL and 222+/-21 fmol/g, n=7). CysA treatment increased AT1 receptor protein expression in the aorta (by 251+/-35%), whereas it was reduced in the kidney (by -32+/-4%). Superoxide anion production in aortic segments and kidney thiobarbituric acid-reactive substance (TBARS) contents were higher in CysA-treated rats (26+/-2 counts/min per milligram and 37+/-3 nmol/g) than in vehicle-treated rats (17+/-1 counts/min per milligram and 24+/-3 nmol/g). Concurrent administration of an AT1 receptor antagonist, valsartan (30 mg/kg per day, in drinking water), to CysA-treated rats (n=7) significantly decreased SBP (113+/-4 mm Hg) and prevented increases in vascular superoxide (16+/-2 counts/min per milligram) and kidney TBARS contents (21+/-3 nmol/g). Similarly, treatment with a superoxide dismutase mimetic, 4-hydroxy-2,2,6,6,-tetramethylpiperidine-N-oxyl (Tempol; 3 mmol/L in drinking water, n=7), prevented CysA-induced increases in SBP (115+/-3 mm Hg), vascular superoxide (16+/-1 counts/min per milligram), and kidney TBARS contents (19+/-2 nmol/g). These data suggest that ROS generation induced by augmented Ang II levels contributes to the development of CysA-induced hypertension.

Indexed as

Angiotensin IIAngiotensin Receptor AntagonistsAnimalsAntioxidantsBlood PressureCreatinineCyclic N-OxidesCyclosporineHypertensionImmunosuppressive AgentsMaleProteinuriaRatsRats, Sprague-DawleyReactive Oxygen SpeciesReceptor, Angiotensin, Type 1Angiotensin IIAngiotensin Receptor AntagonistsAntioxidantsCreatinineCyclic N-OxidesCyclosporineImmunosuppressive AgentsReactive Oxygen SpeciesReceptor, Angiotensin, Type 1Spin LabelstempolTetrazolesValineValsartan

Identifiers

PMID12874088
PMCPMC2572573
OpenAlexW2137730916

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.