Small-conductance calcium-activated potassium current modulates the ventricular escape rhythm in normal rabbit hearts.


Journal

Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317

Informations de publication

Date de publication:
04 2019
Historique:
received: 28 08 2018
pubmed: 18 11 2018
medline: 6 10 2020
entrez: 17 11 2018
Statut: ppublish

Résumé

The apamin-sensitive small-conductance calcium-activated K (SK) current I The purpose of this study was to test the hypothesis that I We tested the effects of apamin (100 nM) on ventricular escape rhythms in Langendorff-perfused rabbit ventricles with atrioventricular block (protocol 1) and on recorded transmembrane action potential of pseudotendons of superfused right ventricular endocardial preparations (protocol 2). All preparations exhibited spontaneous ventricular escape rhythms. In protocol 1, apamin decreased the atrial rate from 186.2 ± 18.0 bpm to 163.8 ± 18.7 bpm (N = 6; P = .006) but accelerated the ventricular escape rate from 51.5 ± 10.7 bpm to 98.2 ± 25.4 bpm (P = .031). Three preparations exhibited bursts of nonsustained ventricular tachycardia and pauses, resulting in repeated burst termination pattern. In protocol 2, apamin increased the ventricular escape rate from 70.2 ± 13.1 bpm to 110.1 ± 2.2 bpm (P = .035). Spontaneous phase 4 depolarization was recorded from the pseudotendons in 6 of 10 preparations at baseline and in 3 in the presence of apamin. There were no changes of phase 4 slope (18.37 ± 3.55 mV/s vs 18.93 ± 3.26 mV/s, N = 3; P = .231, ), but the threshold of phase 0 activation (mV) reduced from -67.97 ± 1.53 to -75.26 ± 0.28 (P = .034). Addition of JTV-519, a ryanodine receptor 2 stabilizer, in 5 preparations reduced escape rate back to baseline. Contrary to its bradycardic effect in the sinus node, I

Sections du résumé

BACKGROUND
The apamin-sensitive small-conductance calcium-activated K (SK) current I
OBJECTIVE
The purpose of this study was to test the hypothesis that I
METHODS
We tested the effects of apamin (100 nM) on ventricular escape rhythms in Langendorff-perfused rabbit ventricles with atrioventricular block (protocol 1) and on recorded transmembrane action potential of pseudotendons of superfused right ventricular endocardial preparations (protocol 2).
RESULTS
All preparations exhibited spontaneous ventricular escape rhythms. In protocol 1, apamin decreased the atrial rate from 186.2 ± 18.0 bpm to 163.8 ± 18.7 bpm (N = 6; P = .006) but accelerated the ventricular escape rate from 51.5 ± 10.7 bpm to 98.2 ± 25.4 bpm (P = .031). Three preparations exhibited bursts of nonsustained ventricular tachycardia and pauses, resulting in repeated burst termination pattern. In protocol 2, apamin increased the ventricular escape rate from 70.2 ± 13.1 bpm to 110.1 ± 2.2 bpm (P = .035). Spontaneous phase 4 depolarization was recorded from the pseudotendons in 6 of 10 preparations at baseline and in 3 in the presence of apamin. There were no changes of phase 4 slope (18.37 ± 3.55 mV/s vs 18.93 ± 3.26 mV/s, N = 3; P = .231, ), but the threshold of phase 0 activation (mV) reduced from -67.97 ± 1.53 to -75.26 ± 0.28 (P = .034). Addition of JTV-519, a ryanodine receptor 2 stabilizer, in 5 preparations reduced escape rate back to baseline.
CONCLUSION
Contrary to its bradycardic effect in the sinus node, I

Identifiants

pubmed: 30445170
pii: S1547-5271(18)31119-6
doi: 10.1016/j.hrthm.2018.10.033
pmc: PMC6443460
mid: NIHMS1522487
pii:
doi:

Substances chimiques

Ryanodine Receptor Calcium Release Channel 0
Small-Conductance Calcium-Activated Potassium Channels 0
Apamin 24345-16-2

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

615-623

Subventions

Organisme : NHLBI NIH HHS
ID : R01 HL139829
Pays : United States
Organisme : NIDA NIH HHS
ID : R42 DA043391
Pays : United States
Organisme : NCATS NIH HHS
ID : U18 TR002208
Pays : United States

Informations de copyright

Copyright © 2018 Heart Rhythm Society. Published by Elsevier Inc. All rights reserved.

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Auteurs

Juyi Wan (J)

Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiothoracic Surgery, the Affiliated Hospital of Southwest Medical University, Luzhou, Sichuan Province, China.

Mu Chen (M)

Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiology, Xinhua Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.

Zhuo Wang (Z)

Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana; Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China.

Thomas H Everett (TH)

Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana.

Michael Rubart-von der Lohe (M)

Department of Pediatrics, Indiana University School of Medicine, Indianapolis, Indiana.

Changyu Shen (C)

Richard and Susan Smith Center for Outcomes Research in Cardiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts.

Zhilin Qu (Z)

Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at the University of California, Los Angeles, California.

James N Weiss (JN)

Departments of Medicine (Cardiology) and Physiology, David Geffen School of Medicine at the University of California, Los Angeles, California.

Penelope A Boyden (PA)

Department of Pharmacology, Columbia University, New York, New York.

Peng-Sheng Chen (PS)

Krannert Institute of Cardiology and Division of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana. Electronic address: chenpp@iu.edu.

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Classifications MeSH