Disconnected Cardiac Autonomic Nerves in Genetic Ganglionic Acetylcholine Receptor Alpha-3 Subunit Deficiency.

Karsten Heusser,Florian Erger, Ulrich Ebner, Barbara Namer,Graeme Eisenhofer, Carl-Albrecht Haensch,Henning Weis, Matthias Schmidt,Alexander Drzezga,Jens Tank,Christian Netzer,Jens Jordan

Hypertension (Dallas, Tex. : 1979)(2023)

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HomeHypertensionVol. 80, No. 8Disconnected Cardiac Autonomic Nerves in Genetic Ganglionic Acetylcholine Receptor Alpha-3 Subunit Deficiency No AccessResearch ArticleRequest AccessFull TextAboutView Full TextView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toNo AccessResearch ArticleRequest AccessFull TextDisconnected Cardiac Autonomic Nerves in Genetic Ganglionic Acetylcholine Receptor Alpha-3 Subunit Deficiency Karsten Heusser, Florian Erger, Ulrich Ebner, Barbara Namer, Graeme Eisenhofer, Carl-Albrecht Haensch, Henning Weis, Matthias Schmidt, Alexander Drzezga, Jens Tank, Christian Netzer and Jens Jordan Karsten HeusserKarsten Heusser https://orcid.org/0000-0002-2571-5585 Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany (K.H., H.W., J.T., J.J.). *K. Heusser and F. Erger contributed equally. Search for more papers by this author , Florian ErgerFlorian Erger https://orcid.org/0000-0002-2768-1702 Institute of Human Genetics, Medical Faculty, University of Cologne, Germany (F.E., C.N.). *K. Heusser and F. Erger contributed equally. Search for more papers by this author , Ulrich EbnerUlrich Ebner https://orcid.org/0009-0002-4648-8497 Internal Medicine Practice, Regensburg, Germany (U.E.). Search for more papers by this author , Barbara NamerBarbara Namer https://orcid.org/0000-0001-7500-2842 Institute of Physiology and Pathophysiology, Friedrich Alexander University Erlangen-Nuremberg, Germany (B.N.). Research Group Neuroscience, Interdisciplinary Centre for Clinical Research within the Faculty of Medicine at the RWTH Aachen University, Germany (B.N.). Department for Physiology, Faculty of Medicine at the RWTH Aachen University, Germany (B.N.). Search for more papers by this author , Graeme EisenhoferGraeme Eisenhofer Institute of Clinical Chemistry and Laboratory Medicine (G.E.), University Hospital Carl Gustav Carus, Medical Faculty, Technical University Dresden, Germany. University Hospital Carl Gustav Carus, Medical Faculty Carl Gustav Carus and Department of Medicine III (G.E.), University Hospital Carl Gustav Carus, Medical Faculty, Technical University Dresden, Germany. Search for more papers by this author , Carl-Albrecht HaenschCarl-Albrecht Haensch https://orcid.org/0000-0001-6479-0265 Kliniken Maria Hilf Mönchengladbach, Autonomic Laboratory, Department of Neurology, Faculty of Health, University of Witten/Herdecke, Mönchengladbach, Germany (C.-A.H.). Search for more papers by this author , Henning WeisHenning Weis https://orcid.org/0000-0001-8638-3281 Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany (K.H., H.W., J.T., J.J.). Department of Nuclear Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany (H.W., M.S., A.D.). Search for more papers by this author , Matthias SchmidtMatthias Schmidt https://orcid.org/0000-0002-7519-8897 Department of Nuclear Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany (H.W., M.S., A.D.). Search for more papers by this author , Alexander DrzezgaAlexander Drzezga Department of Nuclear Medicine, Faculty of Medicine and University Hospital Cologne, University of Cologne, Germany (H.W., M.S., A.D.). Search for more papers by this author , Jens TankJens Tank https://orcid.org/0000-0002-5672-1187 Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany (K.H., H.W., J.T., J.J.). Search for more papers by this author , Christian NetzerChristian Netzer Institute of Human Genetics, Medical Faculty, University of Cologne, Germany (F.E., C.N.). †C. Netzer and J. Jordan contributed equally. Search for more papers by this author and Jens JordanJens Jordan Correspondence to: Jens Jordan, Institute for Aerospace Medicine, Linder Hoehe, 51147 Cologne, Germany. Email E-mail Address: [email protected] https://orcid.org/0000-0003-4518-0706 Institute of Aerospace Medicine, German Aerospace Center (DLR), Cologne, Germany (K.H., H.W., J.T., J.J.). †C. Netzer and J. Jordan contributed equally. Search for more papers by this author Originally published10 May 2023https://doi.org/10.1161/HYPERTENSIONAHA.123.21172Hypertension. 2023;80:e137–e139Footnotes*K. Heusser and F. Erger contributed equally.†C. Netzer and J. Jordan contributed equally.For Sources of Funding and Disclosures, see page e139.Correspondence to: Jens Jordan, Institute for Aerospace Medicine, Linder Hoehe, 51147 Cologne, Germany. Email jens.jordan@dlr.deREFERENCES1. Vernino S, Low PA, Fealey RD, Stewart JD, Farrugia G, Lennon VA. Autoantibodies to ganglionic acetylcholine receptors in autoimmune autonomic neuropathies.N Engl J Med. 2000; 343:847–855. doi: 10.1056/NEJM200009213431204CrossrefMedlineGoogle Scholar2. Schroeder C, Vernino S, Birkenfeld AL, Tank J, Heusser K, Lipp A, Benter T, Lindschau C, Kettritz R, Luft FC, et al. Plasma exchange for primary autoimmune autonomic failure.N Engl J Med. 2005; 353:1585–1590. doi: 10.1056/NEJMoa051719CrossrefMedlineGoogle Scholar3. Shibao CA, Joos K, Phillips JA, Cogan J, Newman JH, Hamid R, Meiler J, Capra J, Sheehan J, Vetrini F, et al. Familial autonomic ganglionopathy caused by rare CHRNA3 genetic variants.Neurology. 2021; 97:e145–e155. doi: 10.1212/WNL.0000000000012143CrossrefMedlineGoogle Scholar4. Mann N, Kause F, Henze EK, Gharpure A, Shril S, Connaughton DM, Nakayama M, Klämbt V, Majmundar AJ, Wu C-HW, et al. CAKUT and autonomic dysfunction caused by acetylcholine receptor mutations.Am J Hum Genet. 2019; 105:1286–1293. doi: 10.1016/j.ajhg.2019.10.004CrossrefMedlineGoogle Scholar5. Rassadi S, Krishnaswamy A, Pié B, McConnell R, Jacob MH, Cooper E. A null mutation for the α3 nicotinic acetylcholine (ACh) receptor gene abolishes fast synaptic activity in sympathetic ganglia and reveals that ACh output from developing preganglionic terminals is regulated in an activity-dependent retrograde manner.J Neurosci. 2005; 25:8555–8566. doi: 10.1523/JNEUROSCI.1983-05.2005CrossrefMedlineGoogle Scholar eLetters(0)eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.Sign In to Submit a Response to This Article Previous Back to top Next FiguresReferencesRelatedDetails August 2023Vol 80, Issue 8 Advertisement Article InformationMetrics © 2023 American Heart Association, Inc.https://doi.org/10.1161/HYPERTENSIONAHA.123.21172PMID: 37161764 Originally publishedMay 10, 2023 Keywordsautonomic nervous systemCHRNA3ganglionic acetylcholine receptorautonomic failurePDF download Advertisement SubjectsAutonomic Nervous SystemGeneticsMechanismsNuclear Cardiology and PETPathophysiology
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