Evidence map›Paper›PMID 8818336›Full record

ArticleBritish journal of pharmacology1996

Modification of aortic contractility in the cardiomyopathic hamster.

E C Dumont, C Lambert, D Lamontagne

Open access · bronzeAbstract read
In one paragraph

Article in British journal of pharmacology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

1 citing paper in PubMed, 6 citations in OpenAlex.

  1. Hypotension in hereditary cardiomyopathy.Pflugers Archiv : European journal of physiology · 2022
    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

3 authors at 1 institution in 1 country.

E C DumontFaculté de pharmacie, Université de Montréal, Québec, Canada.
C Lambert
D Lamontagne
Université de Montréal · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

1. The functional arterial response in the cardiomyopathic hamster compared with inbred control, was investigated in thoracic aortae. For this purpose, vessels were cut into 6-mm rings and mounted in 20-ml organ baths. 2. In a first experimental series, the function of the endothelium was evaluated. Dose-response curves to acetylcholine (0.1 nM-10 microM) on phenylephrine (0.3 microM)-preconstricted rings of cardiomyopathic hamsters and inbred age-matched controls were comparable (log[EC50] of -7.08 +/- 0.12 and -7.18 +/- 0.12, respectively; n = 4). 3. Changes in contractility of cardiomyopathic hamster endothelium-denuded aortae were investigated. Dose-response curves to phenylephrine (1 nM-0.1 mM), angiotensin II (10 pM-0.3 microM), 5-hydroxytryptamine (5-HT) (1 nM-0.1 mM) and KCl (1 mM-0.1 M) were performed. Increased sensitivity in cardiomyopathic hamster aortae, compared to controls, was observed with phenylephrine (log[EC50] of -7.25 +/- 0.05 and -6.83 +/- 0.05, respectively, n = 6, P < 0.001) and angiotensin II (log[EC50] of -8.67 +/- 0.07 and -8.26 +/- 0.06, respectively, n = 6, P = 0.001) but not with 5-HT or KCl. A decreased maximum response in cardiomyopathic, compared to control, was observed with 5-HT (1.28 +/- 0.06 g vs 1.56 +/- 0.07 g, respectively, n = 6, P = 0.03). Comparable results were found in aortae with an intact endothelium. 4. No difference in the maximum contractile response to the G-protein activator, NaF (3, 10 and 30 mM) was observed in either group of animals. 5. Phorbol 12-myristate 13-acetate (PMA, 1-10 microM) was used to assess changes in the activity of protein kinase C (PKC). Contractility to PMA was increased in cardiomyopathic hamster aortae compared to controls (0.22 +/- 0.02 g vs 0.07 +/- 0.03 g at 3 microM, respectively, n = 6, P = 0.003). 6. Finally, cardiomyopathic hamsters aortae were found to be less sensitive when exposed to increasing concentrations of Ca2+ (10 microM-1 mM) in KCl-depolarized rings (0.58 +/- 0.04 g in cardiomyopathic vs 0.79 +/- 0.06 g in control aortae at 0.3 mM, n = 8, P = 0.03). 7. In conclusion, aortae from cardiomyopathic hamsters are more sensitive to phenylephrine and angiotensin II, but not to 5-HT, than those of controls. The increase in sensitivity does not implicate Ca2+ channels or Ca2+ itself since cardiomyopathic hamsters aortae are not more sensitive to KCl- and Ca(2+)-induced contraction. The greater effect of PMA on cardiomyopathic hamster aortae suggests that the increase in sensitivity to phenylephrine and angiotensin II involves an enhanced activity of PKC.

Indexed as

AcetylcholineAngiotensin IIAnimalsAorta, ThoracicCricetinaeDisease Models, AnimalDose-Response Relationship, DrugEndothelium, VascularFemaleMaleMuscle, Smooth, VascularMyocardial ContractionPotassium ChlorideProtein Kinase CSignal TransductionSodium FluorideAcetylcholineAngiotensin IIPotassium ChlorideProtein Kinase CSodium FluorideVasoconstrictor Agents

Identifiers

PMID8818336
PMCPMC1909589
OpenAlexW1964594733

What OpenQuestion holds

Textmetadata
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Registered trials

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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.