Small-conductance calcium-activated potassium current modulates the ventricular escape rhythm in normal rabbit hearts.
Action Potentials
/ physiology
Animals
Apamin
/ pharmacology
Atrioventricular Block
/ drug therapy
Purkinje Fibers
/ physiology
Rabbits
Ryanodine Receptor Calcium Release Channel
/ drug effects
Small-Conductance Calcium-Activated Potassium Channels
/ drug effects
Tachycardia, Ventricular
/ physiopathology
Automaticity
Calcium clock
Idioventricular rhythm
Purkinje cells
Purkinje fibers
Ryanodine receptor
Ventricular tachycardia
Journal
Heart rhythm
ISSN: 1556-3871
Titre abrégé: Heart Rhythm
Pays: United States
ID NLM: 101200317
Informations de publication
Date de publication:
04 2019
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
615-623Subventions
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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