Evidence map›Paper›PMID 26259590›Full record

ArticleHypertension (Dallas, Tex. : 1979)2015

AT2R autoantibodies block angiotensin II and AT1R autoantibody-induced vasoconstriction.

Campbell Liles, Hongliang Li, Vineet Veitla, Jonathan T Liles, Taylor A Murphy, Madeleine W Cunningham, Xichun Yu, David C Kem

Open access · bronzeAbstract read
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 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Observational
  2. Article
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  11. Angiotensin II Type 1 Receptor Autoantibodies in Primary Aldosteronism.Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme · 2020
    Review
  12. Article
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  14. Protective Effect and Mechanism of Alprostadil in Acute Respiratory Distress Syndrome Induced by Oleic Acid in Rats.Medical science monitor : international medical journal of experimental and clinical research · 2018
    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

8 authors at 1 institution in 1 country.

Campbell LilesFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Hongliang LiFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Vineet VeitlaFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Jonathan T LilesFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Taylor A MurphyFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Madeleine W CunninghamFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
Xichun YuFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City.
David C KemFrom the Endocrinology & Heart Rhythm Institute, Department of Medicine (C.L., H. L., V.V., J.T.L., T.A.M., X.Y., D.C.K.) and Department of Microbiology and Immunology (M.W.C.), University of Oklahoma Health Sciences Center and Veterans Affairs Medical Center, Oklahoma City. david-kem@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
Atrial Fibrillation in Hyperthyroidism: Active Antibodies to Autonomic ReceptorsI01CX000381 · VA · OKLAHOMA CITY VA MEDICAL CENTER · PI KEM, DAVID · 2011 to 2013
–
CSRD VA I01 CX000381NHLBI NIH HHS R01 HL056267NIGMS NIH HHS GM092238PHS HHS U26IHS300412
6 · The paper itself

Abstract

Activating autoantibodies to the angiotensin type 1 receptor (AT1R) are associated with hypertensive disorders. The angiotensin type 2 receptor (AT2R) is known to counter-regulate the actions of AT1R. We investigated whether AT2R autoantibodies produced in immunized rabbits will activate AT2R and suppress the vasopressor responses to angiotensin II and AT1R-activating autoantibodies. Five rabbits immunized with a peptide corresponding to the second extracellular loop of AT2R developed high AT2R antibody titers. Rabbit anti-AT2R sera failed to directly dilate isolated rat cremaster arterioles; however, when co-perfused with angiotensin II or AT1R-activating autoantibodies, the anti-AT2R sera significantly inhibited their contractile effects. Rabbit anti-AT2R sera recognized a predominant sequence near the N-terminus of the AT2R second extracellular loop. A decoy peptide based on this sequence effectively reversed the opposing effect of the anti-AT2R sera on angiotensin II-induced contraction of rat cremaster arterioles. A similar blockade of the anti-AT2R sera effect was observed with the AT2R antagonist PD 123319 and the guanylyl cyclase inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one. Rabbit anti-AT2R sera reacted specifically with AT2R. No cross-reactivity with AT1R was observed. Blood pressure did not change in immunized animals. However, the pressor responses to incremental angiotensin II infusions were blunted in immunized animals. Thirteen subjects with primary aldosteronism demonstrated increased AT2R autoantibody levels compared with normal controls. In conclusion, AT2R autoantibodies produced in immunized rabbits have the ability to activate AT2R and counteract the AT1R-mediated vasoconstriction. These autoantibodies provide useful and selective tools for the study of their roles in blood pressure regulation and possible therapeutic intervention.

Indexed as

Angiotensin IIAnimalsAntibodies, BlockingArteriolesAutoantibodiesDisease Models, AnimalEnzyme-Linked Immunosorbent AssayHumansHypertensionMaleRabbitsRatsReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2VasoconstrictionAngiotensin IIAntibodies, BlockingAutoantibodiesReceptor, Angiotensin, Type 1Receptor, Angiotensin, Type 2angiotensin II type 1 receptorangiotensin II type 2 receptorhypertensionrabbitvasoconstriction

Identifiers

PMID26259590
PMCPMC4567423
OpenAlexW1935351823

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.