Contribution of ion currents to beat-to-beat variability of action potential duration in canine ventricular myocytes View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2014-08-02

AUTHORS

Norbert Szentandrássy, Kornél Kistamás, Bence Hegyi, Balázs Horváth, Ferenc Ruzsnavszky, Krisztina Váczi, János Magyar, Tamás Bányász, András Varró, Péter P. Nánási

ABSTRACT

Although beat-to-beat variability (short-term variability, SV) of action potential duration (APD) is considered as a predictor of imminent cardiac arrhythmias, the underlying mechanisms are still not clear. In the present study, therefore, we aimed to determine the role of the major cardiac ion currents, APD, stimulation frequency, and changes in the intracellular Ca2+ concentration ([Ca2+]i) on the magnitude of SV. Action potentials were recorded from isolated canine ventricular cardiomyocytes using conventional microelectrode techniques. SV was an exponential function of APD, when APD was modified by current injections. Drug effects were characterized as relative SV changes by comparing the drug-induced changes in SV to those in APD according to the exponential function obtained with current pulses. Relative SV was increased by dofetilide, HMR 1556, nisoldipine, and veratridine, while it was reduced by BAY K8644, tetrodotoxin, lidocaine, and isoproterenol. Relative SV was also increased by increasing the stimulation frequency and [Ca2+]i. In summary, relative SV is decreased by ion currents involved in the negative feedback regulation of APD (ICa, IKs, and IKr), while it is increased by INa and Ito. We conclude that drug-induced effects on SV should be evaluated in relation with the concomitant changes in APD. Since relative SV was decreased by ion currents playing critical role in the negative feedback regulation of APD, blockade of these currents, or the beta-adrenergic pathway, may carry also some additional proarrhythmic risk in addition to their well-known antiarrhythmic action. More... »

PAGES

1431-1443

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00424-014-1581-4

DOI

http://dx.doi.org/10.1007/s00424-014-1581-4

DIMENSIONS

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PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/25081243


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34 schema:description Although beat-to-beat variability (short-term variability, SV) of action potential duration (APD) is considered as a predictor of imminent cardiac arrhythmias, the underlying mechanisms are still not clear. In the present study, therefore, we aimed to determine the role of the major cardiac ion currents, APD, stimulation frequency, and changes in the intracellular Ca2+ concentration ([Ca2+]i) on the magnitude of SV. Action potentials were recorded from isolated canine ventricular cardiomyocytes using conventional microelectrode techniques. SV was an exponential function of APD, when APD was modified by current injections. Drug effects were characterized as relative SV changes by comparing the drug-induced changes in SV to those in APD according to the exponential function obtained with current pulses. Relative SV was increased by dofetilide, HMR 1556, nisoldipine, and veratridine, while it was reduced by BAY K8644, tetrodotoxin, lidocaine, and isoproterenol. Relative SV was also increased by increasing the stimulation frequency and [Ca2+]i. In summary, relative SV is decreased by ion currents involved in the negative feedback regulation of APD (ICa, IKs, and IKr), while it is increased by INa and Ito. We conclude that drug-induced effects on SV should be evaluated in relation with the concomitant changes in APD. Since relative SV was decreased by ion currents playing critical role in the negative feedback regulation of APD, blockade of these currents, or the beta-adrenergic pathway, may carry also some additional proarrhythmic risk in addition to their well-known antiarrhythmic action.
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42 Ca2
43 HMR 1556
44 ITO
45 InAs
46 K8644
47 SV
48 action
49 action potential duration
50 action potentials
51 addition
52 additional proarrhythmic risk
53 antiarrhythmic action
54 arrhythmias
55 beat variability
56 beats
57 beta-adrenergic pathway
58 blockade
59 canine ventricular cardiomyocytes
60 canine ventricular myocytes
61 cardiac arrhythmias
62 cardiac ion currents
63 cardiomyocytes
64 changes
65 concentration
66 concomitant changes
67 contribution
68 conventional microelectrode techniques
69 critical role
70 current
71 current injection
72 current pulses
73 dofetilide
74 drug effects
75 drug-induced changes
76 drug-induced effects
77 duration
78 effect
79 exponential function
80 feedback regulation
81 frequency
82 function
83 imminent cardiac arrhythmias
84 injection
85 intracellular Ca2
86 ion current
87 isoproterenol
88 lidocaine
89 magnitude
90 magnitude of Sv
91 major cardiac ion currents
92 mechanism
93 microelectrode techniques
94 myocytes
95 negative feedback regulation
96 nisoldipine
97 pathway
98 potential
99 potential duration
100 predictors
101 present study
102 proarrhythmic risk
103 pulses
104 regulation
105 relation
106 relative SV
107 risk
108 role
109 stimulation frequency
110 study
111 summary
112 technique
113 tetrodotoxin
114 variability
115 ventricular cardiomyocytes
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