Evidence map›Paper›PMID 26799746›Full record

ArticlePloS one2016

Vascular Endothelium-Dependent and Independent Actions of Oleanolic Acid and Its Synthetic Oleanane Derivatives as Possible Mechanisms for Hypotensive Effects.

Hlengiwe P Madlala, Thomas Metzinger, Fanie R van Heerden, Cephas T Musabayane, Kanigula Mubagwa, Chantal Dessy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 22% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

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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

6 authors at 3 institutions in 2 countries.

Hlengiwe P MadlalaSchool of Laboratory Medicine & Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa.
Thomas MetzingerPole of Pharmacology and Therapeutics, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
Fanie R van HeerdenSchool of Chemistry & Physics, College of Agriculture, Engineering & Science, University of KwaZulu-Natal, Pietermaritzburg, South Africa.
Cephas T MusabayaneSchool of Laboratory Medicine & Medical Sciences, College of Health Sciences, University of KwaZulu-Natal, Durban, South Africa.
Kanigula MubagwaDepartment of Cardiovascular Sciences, Katholieke Universiteit Leuven, Leuven, Belgium.
Chantal DessyPole of Pharmacology and Therapeutics, Institute of Experimental and Clinical Research, Université catholique de Louvain, Brussels, Belgium.
University of KwaZulu-Natal · ZAUCLouvain · BEKU Leuven · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposePlant-derived oleanolic acid (OA) and its related synthetic derivatives (Br-OA and Me-OA) possess antihypertensive effects in experimental animals. The present study investigated possible underlying mechanisms in rat isolated single ventricular myocytes and in vascular smooth muscles superfused at 37°C.

methodsCell shortening was assessed at 1 Hz using a video-based edge-detection system and the L-type Ca2+ current (ICaL) was measured using the whole-cell patch-clamp technique in single ventricular myocytes. Isometric tension was measured using force transducer in isolated aortic rings and in mesenteric arteries. Vascular effects were measured in endothelium-intact and denuded vessels in the presence of various enzyme or channel inhibitors.

resultsOA and its derivatives increased cell shortening in cardiomyocytes isolated from normotensive rats but had no effect in those isolated from hypertensive animals. These triterpenes also caused relaxation in aortic rings and in mesenteric arteries pre-contracted with either phenylephrine or KCl-enriched solution. The relaxation was only partially inhibited by endothelium denudation, and also partly inhibited by the cyclooxygenase (COX) inhibitor indomethacin, with no additional inhibitory effect of the NO synthase inhibitor, N-ω-Nitro-L-arginine. A combination of both ATP-dependent channel inhibition by glibenclaminde and voltage-dependent K+ channel inhibition by 4-aminopyridine was necessary to fully inhibit the relaxation.

conclusionThese data indicate that the effects of OA and its derivatives are mediated via both endothelium-dependent and independent mechanisms suggesting the involvement of COX in the endothelium-dependent effects and of vascular muscle K+ channels in the endothelium-independent effects. Finally, our results support the view that the antihypertensive action of OA and its derivatives is due to a decrease of vascular resistance with no negative inotropic effect on the heart.

Indexed as

AnimalsAntihypertensive AgentsEndothelium, VascularHypertensionHypotensionIndomethacinMaleMuscle CellsMuscle, Smooth, VascularNitroarginineOleanolic AcidPhenylephrinePotassium ChannelsPotassium ChlorideProstaglandin-Endoperoxide SynthasesRatsAntihypertensive AgentsIndomethacinNitroarginineOleanolic AcidPhenylephrinePotassium ChannelsPotassium ChlorideProstaglandin-Endoperoxide Synthases

Identifiers

PMID26799746
PMCPMC4723044
OpenAlexW2440713773

What OpenQuestion holds

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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.