Evidence map›Paper›PMID 25533964›Full record

ArticleCirculation2015

Paradoxical normoxia-dependent selective actions of inorganic nitrite in human muscular conduit arteries and related selective actions on central blood pressures.

Sami A Omar, Henry Fok, Katharina D Tilgner, Ashok Nair, Joanne Hunt, Benyu Jiang, Paul Taylor, Phil Chowienczyk, Andrew J Webb

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Article in Circulation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

33 citing papers in PubMed, 63 citations in OpenAlex.

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  13. Direct cardiac versus systemic effects of inorganic nitrite on human left ventricular function.American journal of physiology. Heart and circulatory physiology · 2021
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 2 institutions in 1 country.

Sami A OmarFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Henry FokFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Katharina D TilgnerFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Ashok NairFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Joanne HuntFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Benyu JiangFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Paul TaylorFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Phil ChowienczykFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK.
Andrew J WebbFrom the King's College London British Heart Foundation Centre, Cardiovascular Division, Department of Clinical Pharmacology, London, UK (S.A.O., H.F., A.N., J.H., B.J., P.C., A.J.W.); Division of Women's Health, Women's Health Academic Centre, King's College London and King's Health Partners, London, UK (K.D.T., P.T.); Department of Anaesthetics (A.N.), and Biomedical Research Centre (S.A.O., H.F., A.N., J.H., B.J., P.C., A.W.), Guy's & St. Thomas' NHS Foundation Trust, London, UK. andrew.1.webb@kcl.ac.uk.
King's College London · GBKings Health Partners · GB

Funding

British Heart Foundation FS/11/11/28634British Heart Foundation FS/12/9/29233British Heart Foundation SP/14/8/31352
6 · The paper itself

Abstract

backgroundInorganic nitrite dilates small resistance arterioles via hypoxia-facilitated reduction to vasodilating nitric oxide. The effects of nitrite in human conduit arteries have not been investigated. In contrast to nitrite, organic nitrates are established selective dilators of conduit arteries. METHODS AND

resultsWe examined the effects of local and systemic administration of sodium nitrite on the radial artery (a muscular conduit artery), forearm resistance vessels (forearm blood flow), and systemic hemodynamics in healthy male volunteers (n=43). Intrabrachial sodium nitrite (8.7 μmol/min) increased radial artery diameter by a median of 28.0% (25th and 75th percentiles, 25.7% and 40.1%; P<0.001). Nitrite (0.087-87 μmol/min) displayed conduit artery selectivity similar to that of glyceryl trinitrate (0.013-4.4 nmol/min) over resistance arterioles. Nitrite dose-dependently increased local cGMP production at the dose of 2.6 μmol/min by 1.1 pmol·min(-1)·100 mL(-1) tissue (95% confidence interval, 0.5-1.8). Nitrite-induced radial artery dilation was enhanced by administration of acetazolamide (oral or intra-arterial) and oral raloxifene (P=0.0248, P<0.0001, and P=0.0006, respectively) but was inhibited under hypoxia (P<0.0001) and hyperoxia (P=0.0006) compared with normoxia. Systemic intravenous administration of sodium nitrite (8.7 μmol/min) dilated the radial artery by 10.7% (95% confidence interval, 6.8-14.7) and reduced central systolic blood pressure by 11.6 mm Hg (95% confidence interval, 2.4-20.7), augmentation index, and pulse wave velocity without changing peripheral blood pressure.

conclusionsNitrite selectively dilates conduit arteries at supraphysiological and near-physiological concentrations via a normoxia-dependent mechanism that is associated with cGMP production and is enhanced by acetazolamide and raloxifene. The selective central blood pressure-lowering effects of nitrite have therapeutic potential to reduce cardiovascular events.

Indexed as

AdultAnimalsBlood Flow VelocityBlood PressureDose-Response Relationship, DrugForearmHumansInjections, Intra-ArterialMaleMiddle AgedMuscle, SkeletalOrgan Culture TechniquesRadial ArteryRats, Sprague-DawleySodium NitriteVasodilationSodium Nitritearteriesblood pressurenitritesnitroglycerinvasodilation

Identifiers

PMID25533964
OpenAlexW2078382982

What Socratic 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 Socratic graph.