Aminopyridine Lengthened the Plateau Phase of Action Potentials in Mouse Sinoatrial Node Cells

Gonotkov, Mikhail; Golovko, Vladimir

doi:10.1007/s10517-013-2263-5

Cited by 2 publications

(3 citation statements)

References 7 publications

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“…10B). The contribution of I f to the total AP cycle length in the ascidian heart is similar to that in the rabbit heart (Yaniv et al, 2012) heart (Golovko and Gonotkov, 2014). There are grounds to consider that the I f current flows through the HCN channels hyperpolarized by cyclic nucleotides.…”

Section: Role Of I Fmentioning

confidence: 69%

“…Salvador-Recatala et al, 2006). We have supposed that the CionaK v 4 channels mainly conduct the transient outward K + current I to , which is sensitive to 4-AP (Cordeiro et al, 2013;Gonotkov and Golovko, 2013). This current is usually activated at V m from -20 up to -50 mV, but it may be recorded as the sum of I to and I K , because it is difficult to discriminate between these currents by electrophysiological methods.…”

Section: Morphofunctional Characteristicsmentioning

confidence: 99%

“…Supplementary information available online at http://jeb.biologists.org/lookup/doi/10.1242/jeb.154641.supplemental Weisbrod et al 2013). Scheme B is compiled from data by Zaza et al (2009), Gonotkov andGolovko (2013) and Golovko and Gonotkov (2014).…”

Section: Competing Interestsmentioning

confidence: 99%

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Pharmacological analysis of the transmembrane action potential configuration in myoepithelial cells of the spontaneously beating heart of the ascidianStyela rustica in vitro

Golovko

Kosevich

Gonotkov

2017

Journal of Experimental Biology

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The mechanisms of action potential (AP) generation in the myoepithelial cells of the tunicate heart are not yet well understood. Here, an attempt was made to elucidate these mechanisms by analyzing the effects of specific blockers of K, Na and Ca currents on the configuration of transmembrane APs and their frequency in the spontaneously beating ascidian heart. In addition, an immunocytochemical analysis of heart myoepithelial cells was performed. Staining with anti-FMRF-amide and anti-tubulin antibodies did not reveal any nerve elements within the heart tube. Treatment with 1 mmol l TEA ( blocker) resulted in depolarization of heart cell sarcolemma by 10 mV, and inhibition of APs generation was recorded after 3 min of exposure. Prior to this moment, the frequency of AP generation in a burst decreased from 16-18 to 2 beats min owing to prolongation of the diastole. After application of ivabradine (3 or 10 µmol l), the spontaneous APs generation frequency decreased by 24%. Based on these results and published data, it is concluded that the key role in the automaticity of the ascidian heart is played by the outward K currents, Na currents, activated hyperpolarization current and a current of unknown nature.

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Section: Role Of I Fmentioning

confidence: 69%

Section: Morphofunctional Characteristicsmentioning

confidence: 99%

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Pharmacological analysis of the transmembrane action potential configuration in myoepithelial cells of the spontaneously beating heart of the ascidianStyela rustica in vitro

Golovko

Kosevich

Gonotkov

2017

Journal of Experimental Biology

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Modification of distinct ion channels differentially modulates Ca2+ dynamics in primary cultured rat ventricular cardiomyocytes

Shen

Zhao

et al. 2017

Sci Rep

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Primary cultured cardiomyocytes show spontaneous Ca2+ oscillations (SCOs) which not only govern contractile events, but undergo derangements that promote arrhythmogenesis through Ca2+ -dependent mechanism. We systematically examined influence on SCOs of an array of ion channel modifiers by recording intracellular Ca2+ dynamics in rat ventricular cardiomyocytes using Ca2+ specific fluorescence dye, Fluo-8/AM. Voltage-gated sodium channels (VGSCs) activation elongates SCO duration and reduces SCO frequency while inhibition of VGSCs decreases SCO frequency without affecting amplitude and duration. Inhibition of voltage-gated potassium channel increases SCO duration. Direct activation of L-type Ca2+ channels (LTCCs) induces SCO bursts while suppressing LTCCs decreases SCO amplitude and slightly increases SCO frequency. Activation of ryanodine receptors (RyRs) increases SCO duration and decreases both SCO amplitude and frequency while inhibiting RyRs decreases SCO frequency without affecting amplitude and duration. The potencies of these ion channel modifiers on SCO responses are generally consistent with their affinities in respective targets demonstrating that modification of distinct targets produces different SCO profiles. We further demonstrate that clinically-used drugs that produce Long-QT syndrome including cisapride, dofetilide, sotalol, and quinidine all induce SCO bursts while verapamil has no effect. Therefore, occurrence of SCO bursts may have a translational value to predict cardiotoxicants causing Long-QT syndrome.

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Aminopyridine Lengthened the Plateau Phase of Action Potentials in Mouse Sinoatrial Node Cells

Cited by 2 publications

References 7 publications

Pharmacological analysis of the transmembrane action potential configuration in myoepithelial cells of the spontaneously beating heart of the ascidianStyela rustica in vitro

Pharmacological analysis of the transmembrane action potential configuration in myoepithelial cells of the spontaneously beating heart of the ascidianStyela rustica in vitro

Modification of distinct ion channels differentially modulates Ca2+ dynamics in primary cultured rat ventricular cardiomyocytes

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