Evidence map›Paper›PMID 8182156›Full record

ArticleThe Journal of clinical investigation1994

Vascular mechanisms of cyclosporin-induced hypertension in the rat.

J B Roullet, H Xue, D A McCarron, S Holcomb, W M Bennett

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in The Journal of clinical investigation, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.5field-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

20 citing papers in PubMed, 113 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Role of hypertension in kidney transplant recipients.Journal of human hypertension · 2021
    Review
  4. Article
  5. Arterial Stiffness in the Heart Disease of CKD.Journal of the American Society of Nephrology : JASN · 2019
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Assessment and management of hypertension in transplant patients.Journal of the American Society of Nephrology : JASN · 2015
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

J B RoulletDivision of Nephrology, Hypertension and Clinical Pharmacology, Oregon Health Sciences University, Portland 97201.
H Xue
D A McCarron
S Holcomb
W M Bennett
Oregon Health & Science University · US

Funding

VITAMIN E ABSORPTION IN HUMANSP30DK040566 · NIDDK · OREGON HEALTH AND SCIENCE UNIVERSITY · 1990 to 1994
–
NIDDK NIH HHS NIDDK P30DK40566-04
6 · The paper itself

Abstract

Numerous studies have explored the pathogenesis of cyclosporin A (CysA)-induced hypertension; however, none has assessed the impact of CysA treatment on resistance arteries in the setting of elevated blood pressure. Therefore, we studied the chronic effect of CysA on rat mesenteric artery resistance vessels (ex vivo). CysA (25 mg/kg per d for 7 d), but not vehicle, significantly raised systolic blood pressure (13.4 +/- 2.2 mmHg, P < 0.003, n = 9 per group). The resistance vessels from CysA-treated rats showed a small but significant decrease in norepinephrine sensitivity (P < 0.03) and a pronounced decrease in endothelium-dependent and -independent relaxation (P < 0.001) compared to controls. Endothelin-1 sensitivity tended to be diminished (P = 0.07). The direct (in vitro) effect of CysA was subsequently evaluated in resistance vessels from nontreated animals (n = 8) and exposed to CysA (2 micrograms/ml) for 24 h. As observed in vivo, CysA significantly decreased endothelium-dependent and -independent relaxations (P < 0.05) and attenuated norepinephrine sensitivity (P = 0.06). Methylene blue, a nitric oxide quencher, significantly inhibited the acetylcholine-induced relaxation in control, but not in CysA vessels, suggesting a selective action of CysA on the nitric oxide pathway. We conclude that CysA-induced hypertension is the consequence of a primary effect on resistance vessel relaxation, not increased vasoconstriction, as previously suggested.

Indexed as

AcetylcholineAnimalsBlood PressureBody WeightCyclosporineDose-Response Relationship, DrugDrug InteractionsEndothelinsHypertensionMaleMesenteric ArteriesMethylene BlueMuscle RelaxationNitroprussideNorepinephrineRatsAcetylcholineCyclosporineEndothelinsMethylene BlueNitroprussideNorepinephrine

Identifiers

PMID8182156
PMCPMC294377
OpenAlexW2001918921

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.