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Sympathetic and vagal interaction in the control of cardiac pacemaker rhythm in the guinea-pig heart: Importance of expressing heart rhythm using an appropriate metric

  • Sherif Elawa
    Affiliations
    Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linköping University, SE-58185 Linköping, Sweden
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  • Robert M. Persson
    Affiliations
    Department of Heart Disease, Haukeland University Hospital, 5021 Bergen, Norway
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  • Su Young Han
    Affiliations
    Department of Physiology, Development and Neuroscience, University of Cambridge, Downing Street, Cambridge CB2 3DY, UK
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  • Author Footnotes
    1 The study was performed at the Department of Physiology, School of Medical Sciences, University of Otago, PO Box 913, Dunedin, 9054, New Zealand.
    Chris P. Bolter
    Correspondence
    Corresponding author.
    Footnotes
    1 The study was performed at the Department of Physiology, School of Medical Sciences, University of Otago, PO Box 913, Dunedin, 9054, New Zealand.
    Affiliations
    Department of Physiology, School of Medical Sciences, University of Otago, 913, Dunedin 9054, New Zealand
    Search for articles by this author
  • Author Footnotes
    1 The study was performed at the Department of Physiology, School of Medical Sciences, University of Otago, PO Box 913, Dunedin, 9054, New Zealand.
Published:September 10, 2022DOI:https://doi.org/10.1016/j.autneu.2022.103025
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      Highlights

      • Illustrated importance of expressing changes in heart rate and heart period as fractions or ratios
      • No evidence for accentuated antagonism in autonomic control of guinea-pig heart rhythm
      • Influence of brief/small vagal input on heart rhythm is reduced by sympathetic stimulation.

      Abstract

      There are many reports that, through pre- and post-junctional mechanisms, sympathetic and parasympathetic (vagal) nerves can interact in the control of heart rate. The predominant interaction is accentuated antagonism (AA), where the bradycardia produced by vagal stimulation (VNS) is amplified when heart rate has been increased by sympathetic stimulation (SNS) or beta-adrenergic agonists. The acetylcholine-activated potassium current (IK,Ach), is the primary driver of vagal bradycardia. To examine the participation of IK,Ach in AA, a series of experiments was performed on isolated, double innervated, guinea-pig atrial preparations. Vagal bradycardia was elicited by 10-s trains (1, 2, 5 and 7.5 Hz) or single bursts of VNS (3 stimuli at 50 Hz) before and during acceleration of HR by either SNS (1–3 Hz) or isoprenaline (ISO), in both absence and presence of tertiapin-Q (TQ–IK,Ach blocker). When expressed as an absolute change in HR (beats/min), bradycardia produced by VNS trains was amplified (AA) at all frequencies of VNS in ISO, and at 5 and 7.5 Hz during SNS. Bradycardia in response to 1 and 2 Hz VNS was reduced during SNS. In TQ, only the bradycardia produced by 5 and 7.5 Hz VNS in ISO was amplified. The bradycardia produced by a single burst of VNS was amplified in both ISO and SNS. After TQ the bradycardia in response to a VNS burst was unchanged in ISO, while it was reduced during SNS. When these data were adjusted to account for the increase in baseline HR brought about by SNS and ISO, there was no longer evidence of AA. Diminished responses to low frequencies of VNS (1 and 2 Hz) persisted, and were also seen during IK,Ach block by TQ. We applied the same adjustment to data from 20 published studies. In 8 studies all data indicated AA; 3 studies provided no evidence for AA, and in 9 studies evidence was mixed. There is no doubt that AA can occur in the control of heart rhythm during simultaneous SNS and VNS, but conditions which determine its occurrence, and the mechanisms involved in this interaction remain unclear.

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