Evidence map›Paper›PMID 25691619›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

Novel retro-inverso peptide inhibitor reverses angiotensin receptor autoantibody-induced hypertension in the rabbit.

Hongliang Li, David C Kem, Ling Zhang, Bing Huang, Campbell Liles, Alexandria Benbrook, Hariprasad Gali, Vineet Veitla, Benjamin J Scherlag, Madeleine W Cunningham and 1 more

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Hypertension (Dallas, Tex. : 1979), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. Transcutaneous vagus nerve stimulation attenuates autoantibody-mediated cardiovagal dysfunction and inflammation in a rabbit model of postural tachycardia syndrome.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2023
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  2. Review
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  9. Novel allosteric ligands of the angiotensin receptor AT1R as autoantibody blockers.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  10. Review
  11. Adrenergic Autoantibody-Induced Postural Tachycardia Syndrome in Rabbits.Journal of the American Heart Association · 2019
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  12. Article
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  15. Article
  16. Method to generate highly stable D-amino acid analogs of bioactive helical peptides using a mirror image of the entire PDB.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  17. Review
  18. A peptidomimetic inhibitor suppresses the inducibility of β1-adrenergic autoantibody-mediated cardiac arrhythmias in the rabbit.Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing · 2015
    Article
  19. 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

11 authors at 1 institution in 1 country.

Hongliang LiFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
David C KemFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Ling ZhangFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Bing HuangFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Campbell LilesFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Alexandria BenbrookFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Hariprasad GaliFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Vineet VeitlaFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Benjamin J ScherlagFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Madeleine W CunninghamFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Xichun YuFrom the Department of Medicine and the Heart Rhythm Institute (H.L., D.C.K., L.Z., B.H., C.L., A.B., V.V., B.J.S., X.Y.), and Departments of Pharmaceutical Sciences (H.G.) and Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City. xichun-yu@ouhsc.edu.
University of Oklahoma Health Sciences Center · US

Funding

AUTOIMMUNE DETERMINANTS OF HUMAN CARDIAC MYOSINR01HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 1997 to 2013
$4.7M
Autoimmune Determinants of Human Cardiac MyosinR56HL056267 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI COOPER, LESLIE T, CUNNINGHAM, MADELEINE W. · 2008 to 2015
$933k
NHLBI NIH HHS HL56267NHLBI NIH HHS R01 HL056267NHLBI NIH HHS R56 HL056267
6 · The paper itself

Abstract

Activating autoantibodies to the angiotensin II type 1 receptor (AT1R) have been implicated in hypertensive disorders. We investigated whether AT1R antibodies produced in immunized rabbits will activate AT1R and contribute to hypertension by a direct contractile effect on the vasculature and whether they can be blocked by a novel decoy peptide. A multiple antigenic peptide containing the AT1R epitope AFHYESQ, which is the receptor-binding epitope of AT1R-activating autoantibodies, was used to immunize 6 rabbits. AT1R antibody activity was analyzed in AT1R-transfected cells, and their contractile effects were assayed using isolated perfused rat cremaster resistance arterioles. A retro-inverso D-amino acid epitope-mimetic peptide was tested for AT1R antibody inhibition in vitro and in vivo. All immunized animals produced high AT1R antibody titers and developed elevated blood pressure. No changes in measured blood chemistry values were observed after immunization. Rabbit anti-AT1R sera induced significant AT1R activation in transfected cells and vasoconstriction in the arteriole assay, both of which were blocked by losartan and the retro-inverso D-amino acid peptide. A single intravenous bolus injection of the retro-inverso d-amino acid peptide (1 mg/kg) into immunized rabbits dropped the mean arterial pressure from 122±11 to 82±6 mm Hg. Rabbit anti-AT1R sera partially suppressed angiotensin II-induced contraction of isolated rat cremaster arterioles, and the pressor response to angiotensin II infusion was attenuated in immunized animals. In conclusion, AT1R-activating autoantibodies and the retro-inverso d-amino acid peptide, respectively, have important etiologic and therapeutic implications in hypertensive subjects who harbor these autoantibodies.

Indexed as

AnimalsAutoantibodiesBlood PressureChromatography, High Pressure LiquidDisease Models, AnimalEnzyme-Linked Immunosorbent AssayHypertensionRabbitsReceptor, Angiotensin, Type 1VasoconstrictionAutoantibodiesReceptor, Angiotensin, Type 1hypertensionrabbitreceptor, angiotensin, type 1retro-inverso peptidevasoconstriction

Identifiers

PMID25691619
PMCPMC4359052
OpenAlexW2118011431

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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.