Evidence map›Paper›PMID 11015303›Full record

ArticleBritish journal of pharmacology2000

Nitric oxide and sodium nitroprusside-induced relaxation of the human umbilical artery.

F Lovren, C Triggle

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

21 citing papers in PubMed, 70 citations in OpenAlex.

  1. Review
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  7. Review
  8. UV-B Filter Octylmethoxycinnamate Induces Vasorelaxation by CaInternational journal of molecular sciences · 2019
    Article
  9. Review
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  11. Article
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  13. Review
  14. Review
  15. Article
  16. Umbilical artery tone in maternal obesity.Reproductive biology and endocrinology : RB&E · 2009
    Article
  17. Article
  18. Article
  19. Article
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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.

F LovrenDepartment of Pharmacology & Therapeutics and Smooth Muscle Research Group, Faculty of Medicine, University of Calgary, Calgary, Alberta, Canada T2N 4N1.
C Triggle
University of Calgary · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the human umbilical artery (HUA) pre-contracted with the thromboxane mimetic U46619 or with 5-hydroxytryptamine (5-HT), (and pretreated with indomethacin (3 microM) to suppress the synthesis of prostanoids), authentic nitric oxide (NO) evoked concentration-dependent relaxation (pEC(50) 7.05 and 5.99, respectively). In contrast, sodium nitroprusside (SNP) induced relaxation only in U46619 pre-contracted HUA (pEC(50) 6.52). At high (>300 mmHg) vs low (<55 mmHg) oxygen tension the dose-response curves to NO- and SNP-induced relaxations were biphasic and shifted leftward. Preincubation of the arterial rings with the soluble guanylyl cyclase (sGC) inhibitor 1H[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one (ODQ; 10 microM) shifted the concentration-response curve to NO, reduced the maximal relaxation response to NO (E(max) 71%) and to SNP (E(max) 10%). Pre-exposure of HUA rings to high extracellular K(+) (50 mM) reduced E(max) relaxation responses to NO (36%) and SNP (1%). Pretreatment of the HUA with the K(+) channel inhibitors, tetraethylammonium (TEA, 1 mM), 4-aminopyridine (4-AP, 0.5 mM), charybdotoxin (0.1 microM) or iberiotoxin (0.1 microM) increased the pEC(30) for NO and SNP and changed the shape of the dose-response curves from biphasic to monophasic. Pre-incubation of HUA rings with TEA (1 mM), 4-AP (0.5 mM) and ODQ (10 microM) significantly reduced the NO-induced maximal relaxation (E(max) 26%) but not the pEC(50) (5.60). These data indicate that SNP-induced relaxation in the HUA is primarily mediated via sGC-cyclic GMP whereas NO-induced relaxation also involves the activation of K(V) and K(Ca) channels and a cyclic GMP/K(+) channel-independent mechanism(s).

Indexed as

Calcium ChannelsCyclic GMPEnzyme InhibitorsGuanylate CyclaseHumansIn Vitro TechniquesNifedipineNitric OxideNitroprussideOxadiazolesOxygenPotassiumPotassium Channel BlockersPotassium ChannelsQuinoxalinesReceptors, Atrial Natriuretic Factor1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-oneatrial natriuretic factor receptor ACalcium ChannelsCyclic GMPEnzyme InhibitorsGuanylate CyclaseNifedipineNitric OxideNitroprussideOxadiazolesOxygenPotassiumPotassium Channel BlockersPotassium ChannelsQuinoxalinesReceptors, Atrial Natriuretic FactorVasodilator Agents

Identifiers

PMID11015303
PMCPMC1572347
OpenAlexW2038021990

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.