Evidence map›Paper›PMID 8486781›Full record

ArticleThe Journal of clinical investigation1993

Effects of endothelin receptor antagonist on cyclosporine-induced vasoconstriction in isolated rat renal arterioles.

D M Lanese, J D Conger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 1 pooled it
5.5field-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

50 citing papers in PubMed, 1 synthesis or guideline pooled it, 221 citations in OpenAlex.

  1. Pooled it
  2. Multitarget therapy with a corticosteroid, cyclosporine and mycophenolate mofetil for idiopathic membranous nephropathy: a prospective randomized controlled trial.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2023
    Trial
  3. Review
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  7. What can we learn from treatments of oral lichen planus?Frontiers in cellular and infection microbiology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. New onset hypertension after transplantation.World journal of transplantation · 2022
    Review
  12. Article
  13. Cognitive Function in Kidney Transplantation.Current transplantation reports · 2020
    Article
  14. Review
  15. The Many Faces of Calcineurin Inhibitor Toxicity-What the FK?Advances in chronic kidney disease · 2020
    Review
  16. 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
  17. Review
  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

2 authors at 1 institution in 1 country.

D M LaneseDepartment of Medicine, University of Colorado Health Sciences Center, Denver.
J D Conger
University of Colorado Health · US

Funding

PATHOGENESIS OF CYCLOSPORIN-INDUCED VASOTOXICITYF32DK008611 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI LANESE, DIANE M · 1991 to 1992
–
VASCULATURE DYNAMIC ABNORMALITIES IN ACUTE RENAL FAILURER01DK041294 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI CONGER, JOHN D · 1989 to 1991
–
NIDDK NIH HHS 5 S32 DK 08611-02NIDDK NIH HHS R01 DK41294
6 · The paper itself

Abstract

Recent evidence suggests that the potent constrictor peptide, endothelin (ET) has a mediating role in cyclosporine A (CsA)-related renal vasoconstriction. However, the nature of the CsA-ET interaction and effect on the renal vasculature is uncertain. The purpose of the present study was twofold: (a) to determine if CsA exposure caused direct local release of ET from the endothelium of the renal microvasculature and (b) to determine if locally generated ET has paracrine effects on the underlying vascular smooth muscle to induce vasoconstriction. Experiments were performed in isolated rat renal arterioles. First it was determined that both afferent arteriole (AA) and efferent arteriole (EA) exhibited concentration-dependent decreases in lumen diameter to increasing molar concentrations of CsA. The AA was more sensitive to the vasoconstrictive effects of CsA than the EA. Next, the blocking effect of a recently synthesized putative ETA receptor antagonist was verified in both the AA and EA, where it was found that the cyclic peptide cyclo D-Asp-L-Pro-D-Val-L-Leu-D-Trp totally inhibited the vasoconstriction observed with ET addition. Finally, the role of locally stimulated ET in CsA-induced vasoconstriction was tested by determining the effect of the ETA receptor antagonist on CsA-induced AA and EA constriction. In the AA the vasoconstrictor effect of 10(-11) M CsA was completely blocked by the ETA receptor antagonist. However, in contrast to AA, 10(-11) M CsA in EA in the presence of the ETA receptor antagonist decreased EA lumen diameter by a mean of 41% from baseline (4.80 +/- 0.75 microns vs 7.80 +/- 0.84 microns, P < 0.05). This change in lumen diameter was similar to that induced by CsA alone. These data suggest that CsA directly constricts renal microvessels. This effect is mediated by ET in the AA but not the EA.

Indexed as

Endothelin Receptor AntagonistsAmino Acid SequenceAnimalsArteriolesCyclosporineDose-Response Relationship, DrugEndothelinsIn Vitro TechniquesKidneyMolecular Sequence DataMuscle, Smooth, VascularOligopeptidesPeptides, CyclicRatsRats, Sprague-DawleyRenal CirculationCyclosporineEndothelin Receptor AntagonistsEndothelinsOligopeptidesPeptides, Cyclic

Identifiers

PMID8486781
PMCPMC288216
OpenAlexW2046221239

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.