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Excitation-contraction coupling in human heart failure examined by action potential clamp in rat cardiac myocytes

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Excitation-contraction coupling in human heart failure examined by action potential clamp in rat cardiac myocytes. / Cooper, P J; Soeller, C; Cannell, MB.

In: Journal of Molecular and Cellular Cardiology, Vol. 49, 12.2010, p. 911 - 917.

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Cooper, P J ; Soeller, C ; Cannell, MB. / Excitation-contraction coupling in human heart failure examined by action potential clamp in rat cardiac myocytes. In: Journal of Molecular and Cellular Cardiology. 2010 ; Vol. 49. pp. 911 - 917.

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@article{46711106c6e04b8ab72c49cf8b889f9a,
title = "Excitation-contraction coupling in human heart failure examined by action potential clamp in rat cardiac myocytes",
abstract = "The effect of the loss of the notch in the human action potential (AP) during heart failure was examined by voltage clamping rat ventricular myocytes with human APs and recording intracellular Ca(2+) with fluorescent dyes. Loss of the notch resulted in about a 50{\%} reduction in the initial phase of the Ca(2+) transient due to reduced ability of the L-type Ca(2+) channel to trigger release. The failing human AP increased non-uniformity of cytosolic Ca(2+), with some cellular regions failing to elicit Ca(2+)-induced Ca(2+) release from the sarcoplasmic reticulum. In addition, there was an increase in the occurrence of late Ca(2+) sparks. Monte-Carlo simulations of spark activation by L-type Ca(2+) current supported the idea that the decreased synchrony of Ca(2+) spark production associated with the loss of the notch could be explained by reduced Ca(2+) influx from open Ca(2+) channels. We conclude that the notch of the AP is critical for efficient and synchronous EC coupling and that the loss of the notch will reduce the SR Ca(2+) release in heart failure, without changes in (for example) SR Ca(2+)-ATPase uptake.",
author = "Cooper, {P J} and C Soeller and MB Cannell",
year = "2010",
month = "12",
doi = "10.1016/j.yjmcc.2010.04.012",
language = "English",
volume = "49",
pages = "911 -- 917",
journal = "Journal of Molecular and Cellular Cardiology",
issn = "0022-2828",
publisher = "Elsevier",

}

RIS - suitable for import to EndNote

TY - JOUR

T1 - Excitation-contraction coupling in human heart failure examined by action potential clamp in rat cardiac myocytes

AU - Cooper, P J

AU - Soeller, C

AU - Cannell, MB

PY - 2010/12

Y1 - 2010/12

N2 - The effect of the loss of the notch in the human action potential (AP) during heart failure was examined by voltage clamping rat ventricular myocytes with human APs and recording intracellular Ca(2+) with fluorescent dyes. Loss of the notch resulted in about a 50% reduction in the initial phase of the Ca(2+) transient due to reduced ability of the L-type Ca(2+) channel to trigger release. The failing human AP increased non-uniformity of cytosolic Ca(2+), with some cellular regions failing to elicit Ca(2+)-induced Ca(2+) release from the sarcoplasmic reticulum. In addition, there was an increase in the occurrence of late Ca(2+) sparks. Monte-Carlo simulations of spark activation by L-type Ca(2+) current supported the idea that the decreased synchrony of Ca(2+) spark production associated with the loss of the notch could be explained by reduced Ca(2+) influx from open Ca(2+) channels. We conclude that the notch of the AP is critical for efficient and synchronous EC coupling and that the loss of the notch will reduce the SR Ca(2+) release in heart failure, without changes in (for example) SR Ca(2+)-ATPase uptake.

AB - The effect of the loss of the notch in the human action potential (AP) during heart failure was examined by voltage clamping rat ventricular myocytes with human APs and recording intracellular Ca(2+) with fluorescent dyes. Loss of the notch resulted in about a 50% reduction in the initial phase of the Ca(2+) transient due to reduced ability of the L-type Ca(2+) channel to trigger release. The failing human AP increased non-uniformity of cytosolic Ca(2+), with some cellular regions failing to elicit Ca(2+)-induced Ca(2+) release from the sarcoplasmic reticulum. In addition, there was an increase in the occurrence of late Ca(2+) sparks. Monte-Carlo simulations of spark activation by L-type Ca(2+) current supported the idea that the decreased synchrony of Ca(2+) spark production associated with the loss of the notch could be explained by reduced Ca(2+) influx from open Ca(2+) channels. We conclude that the notch of the AP is critical for efficient and synchronous EC coupling and that the loss of the notch will reduce the SR Ca(2+) release in heart failure, without changes in (for example) SR Ca(2+)-ATPase uptake.

U2 - 10.1016/j.yjmcc.2010.04.012

DO - 10.1016/j.yjmcc.2010.04.012

M3 - Article

VL - 49

SP - 911

EP - 917

JO - Journal of Molecular and Cellular Cardiology

T2 - Journal of Molecular and Cellular Cardiology

JF - Journal of Molecular and Cellular Cardiology

SN - 0022-2828

ER -