Activated human platelet products induce proarrhythmic effects in ventricular myocytes

Jong, Jonas S.S.G. de; Verkerk, Arie O.; Borren, Marcel M. G. J. van; Zakhrabova-Zwiauer, Olga M; Nieuwland, Rienk; Meijers, Joost C. M.; Akkerman, Jan-Willem Ν.; Wilde, Arthur A.M.; Tan, Hanno L.; Dekker, Lukas

doi:10.1016/j.yjmcc.2011.05.016

Cited by 5 publications

(12 citation statements)

References 47 publications

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“…After excision of the heart from male New Zealand White rabbits 49 , single left atrial and ventricular cells were isolated as described previously, with minor modifications 51 , 52 . In short, hearts were mounted on a Langendorff perfusion apparatus and retrogradely perfused at 37 °C through the aorta with a modified Tyrode’s solution (see above) at a constant pressure (50 mmHg) for 15 min.…”

Section: Methodsmentioning

confidence: 99%

“…Action potentials (APs) and membrane currents were recorded at 36.5 °C with the amphotericin-B-perforated or ruptured patch clamp technique 51 , using an Axopatch 200B Clamp amplifier (Molecular Devices Corporation, Sunnyvale, CA, USA). Voltage control, data acquisition, and analysis were performed using custom-made software.…”

Section: Methodsmentioning

confidence: 99%

“…To accurately determine I to , measurements were performed in the presence of blockers of Na + channels (30 µM tetrodotoxin (TTX)), Ca 2+ channels (0.25 mM CdCl 2 ) and of delayed rectifier K + channels (5 µM E-4031, 100 µM chromanol 293B). 51 For I Cl(Ca) measurements, 10 µM TTX and 2 mM 4-aminopyridine (4-AP) was added to the standard superfusion solution. 57 …”

Section: Methodsmentioning

confidence: 99%

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Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Veldkamp

Geuzebroek²,

Baartscheer

et al. 2018

Nat Commun

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The cardiac autonomic nervous system (ANS) controls normal atrial electrical function. The cardiac ANS produces various neuropeptides, among which the neurokinins, whose actions on atrial electrophysiology are largely unknown. We here demonstrate that the neurokinin substance-P (Sub-P) activates a neurokinin-3 receptor (NK-3R) in rabbit, prolonging action potential (AP) duration through inhibition of a background potassium current. In contrast, ventricular AP duration was unaffected by NK-3R activation. NK-3R stimulation lengthened atrial repolarization in intact rabbit hearts and consequently suppressed arrhythmia duration and occurrence in a rabbit isolated heart model of atrial fibrillation (AF). In human atrial appendages, the phenomenon of NK-3R mediated lengthening of atrial repolarization was also observed. Our findings thus uncover a pathway to selectively modulate atrial AP duration by activation of a hitherto unidentified neurokinin-3 receptor in the membrane of atrial myocytes. NK-3R stimulation may therefore represent an anti-arrhythmic concept to suppress re-entry-based atrial tachyarrhythmias, including AF.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Veldkamp

Geuzebroek²,

Baartscheer

et al. 2018

Nat Commun

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“…De Jong and colleagues have demonstrated that products secreted from activated human platelets induce changes in I Ca,L and [Ca 2+ ] i , which result in action potential prolongation and the occurrence of EAD and DAD in rabbit myocytes [36]. Interestingly, although products of activated platelets consist of organic substrates and more than 2000 proteins, LPA is an important component [37].…”

Section: Discussionmentioning

confidence: 99%

Lysophosphatidic Acid Increases the Electrophysiological Instability of Adult Rabbit Ventricular Myocardium by Augmenting L-Type Calcium Current

Wei

Zhao

et al. 2012

PLoS ONE

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Lysophosphatidic acid (LPA) has diverse actions on the cardiovascular system and is widely reported to modulate multiple ion currents in some cell types. However, little is known about its electrophysiological effects on cardiac myocytes. This study investigated whether LPA has electrophysiological effects on isolated rabbit myocardial preparations. The results indicate that LPA prolongs action potential duration at 90% repolarization (APD90) in a concentration- and frequency-dependent manner in isolated rabbit ventricular myocytes. The application of extracellular LPA significantly increases the coefficient of APD90 variability. LPA increased L-type calcium current (ICa,L) density without altering its activation or deactivation properties. In contrast, LPA has no effect on two other ventricular repolarizing currents, the transient outward potassium current (Ito) and the delayed rectifier potassium current (IK). In arterially perfused rabbit left ventricular wedge preparations, the monophasic action potential duration, QT interval, and Tpeak-end are prolonged by LPA. LPA treatment also significantly increases the incidence of ventricular tachycardia induced by S1S2 stimulation. Notably, the effects of LPA on action potentials and ICa,L are PTX-sensitive, suggesting LPA action requires a Gi-type G protein. In conclusion, LPA prolongs APD and increases electrophysiological instability in isolated rabbit myocardial preparations by increasing ICa,L in a Gi protein-dependent manner.

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“…MI results from thrombotic coronary occlusion. Previously, we reported that activated blood platelet products (ABPP) facilitate VF occurrence by increasing intracellular Ca 2 + (Ca 2 + i ) transients and L-type Ca 2 + current (I Ca,L ) in cardiac myocytes [1]. Trypsin reduced these effects, suggesting involvement of peptides.…”

mentioning

confidence: 95%

Acetylsalicylic acid prevents platelet-induced proarrhythmic effects on intracellular Ca2+ homeostasis in ventricular myocytes

Zakhrabova-Zwiauer

Verkerk

Jong

et al. 2013

International Journal of Cardiology

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Activated human platelet products induce proarrhythmic effects in ventricular myocytes

Cited by 5 publications

References 47 publications

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Neurokinin-3 receptor activation selectively prolongs atrial refractoriness by inhibition of a background K+ channel

Lysophosphatidic Acid Increases the Electrophysiological Instability of Adult Rabbit Ventricular Myocardium by Augmenting L-Type Calcium Current

Acetylsalicylic acid prevents platelet-induced proarrhythmic effects on intracellular Ca2+ homeostasis in ventricular myocytes

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