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Cited by 24Cardiac electrophysiology and arrhythmiasHeart Rate Variability and Autonomic ControlCardiac Arrhythmias and Treatments

The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.

Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties.

Open access
Nayebpour, M, Talajic, M, Nattel, S·1992·Circulation Research
DOI 10.1161/01.res.70.5.902
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Abstract

Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.

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Crossref · 10.1161/01.res.70.5.902

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  • β-blockers and non-DHP CCBs exert their negative dromotropic effects primarily at the level of the AV node.

    “Β‐blockers and non‐DHP CCBs exert their negative dromotropic effects primarily at the level of the AV node [15, 16].”

    From Clinical Significance and Management of Atrioventricular Block Associated With Bradycardic/Antiarrhythmic Drug Therapy: Drug-Induced or Drug-Revealed? (2025) · cites this paper as [15]

    The General Effects section reports that β-adrenergic blockade slows AV nodal conduction, and the Conclusions describe increased negative dromotropic effects in the AV node during blockade. The paper does not establish that the AV node is the primary site of the effect relative to other sites, and it does not assess non-DHP calcium channel blockers. (LLM, conf=0.87)

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Research works printed but not linked: 8

  1. [1]1. Zipes DP: Specific arrhythmias: Diagnosis and treatment, in Braunwald E (ed): Heart Disease, ed 3. Philadelphia, Pa, WB Saunders Co, 1988, pp 658-716
  2. [4]4. Lewis T, Master AM: Observations upon conduction in the mammalian heart: AV conduction. Heart 1925;12:209-269
  3. [9]9. Simson MB, Spear JF, Moore EN: Electrophysiological studies in AV nodal Wenckebach cycles. Am J Cardiol 1978;41:244-258
  4. [25]25. Rothberger DJ, Winterberg H: Ueber die Beziehung der Herzner- ven zur Automatischen Reizerzeugung und zum Ploetzlechen Herztode. Arch Ges Physiol 1911;141:343-377
  5. [28]28. Lister JW, Stein E, Kosowsky BD, Lau SH, Damato AN: Atrio- ventricular conduction in man. Am J Cardiol 1965;16:516-523
  6. [29]29. Wallace AG, Troyer WG, Lesage MA, Zotti EF: Electrophysio- logic effects of isoproterenol and ,3-blocking agents in awake dogs. Circ Res 1966;18:140-148
  7. [42]42. Prystowsky EN, Page RL: Electrophysiology and autonomic influ- ences of the human atrioventricular node. Prog Clin Biol Res 1988;275:259-277
  8. [55]55. Warner MR, deTarnowsky JM, Whitson CC, Loeb JM: Beat-by- beat modulation of AV conduction: II. Autonomic neural mecha- nisms. Am J Physiol 1986;251:H1134-H1142

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Metadata

Authors
Nayebpour, M., Talajic, M., & Nattel, S.
Affiliations
Montreal Heart Institute (CA)
ORCID
Venue
Circulation Research
Publisher
Ovid Technologies (Wolters Kluwer Health)
Published
1992-05
Volume
70
Issue
5
Pages
902-911
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
DOI
10.1161/01.res.70.5.902
OpenAlex
W2109731804
Cited by
24
References
51
Citations by year
2025: 1 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 2
FWCI
1.46
Type
journal article
Language
en
Open access
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Medical Research Council Canada
  • Fonds de Recherche du Québec - Santé
  • Medical Research Council
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac electrophysiology and arrhythmias
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Heart Rate Variability and Autonomic Control
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Arrhythmias and Treatments
Keywords
beta-adrenergic receptors, sympathetic nervous system, isoproterenol, beta-adrenergic blockade, stellate ganglion stimulation, tachycardia
MeSH terms
Adrenergic beta-Antagonists, Animals, Arrhythmias, Cardiac, Atrioventricular Node, Dogs, Electrocardiography, Female, Heart Rate, Isoproterenol, Male, Models, Cardiovascular, Nadolol, Receptors, Adrenergic, beta, Calcium Channels

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