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本文引用的文献

1
Distinct patterns of constitutive phosphodiesterase activity in mouse sinoatrial node and atrial myocardium.在小鼠窦房结和心房心肌中存在组成型磷酸二酯酶活性的不同模式。
PLoS One. 2012;7(10):e47652. doi: 10.1371/journal.pone.0047652. Epub 2012 Oct 15.
2
Development of cardiac parasympathetic neurons, glial cells, and regional cholinergic innervation of the mouse heart.心脏副交感神经元、神经胶质细胞的发育和小鼠心脏的区域性胆碱能神经支配。
Neuroscience. 2012 Sep 27;221:28-36. doi: 10.1016/j.neuroscience.2012.06.061. Epub 2012 Jul 3.
3
The natriuretic peptides BNP and CNP increase heart rate and electrical conduction by stimulating ionic currents in the sinoatrial node and atrial myocardium following activation of guanylyl cyclase-linked natriuretic peptide receptors.利钠肽 BNP 和 CNP 通过激活与鸟苷酸环化酶偶联的利钠肽受体,刺激窦房结和心房心肌中的离子电流,从而增加心率和电传导。
J Mol Cell Cardiol. 2012 May;52(5):1122-34. doi: 10.1016/j.yjmcc.2012.01.018. Epub 2012 Feb 1.
4
Iron overload decreases CaV1.3-dependent L-type Ca2+ currents leading to bradycardia, altered electrical conduction, and atrial fibrillation.铁过载减少了 CaV1.3 依赖性 L 型钙电流,导致心动过缓、电传导改变和心房颤动。
Circ Arrhythm Electrophysiol. 2011 Oct;4(5):733-42. doi: 10.1161/CIRCEP.110.960401. Epub 2011 Jul 11.
5
Changes in the expression of ion channels, connexins and Ca2+-handling proteins in the sino-atrial node during postnatal development.在出生后发育过程中心房结中离子通道、连接蛋白和 Ca2+处理蛋白表达的变化。
Exp Physiol. 2011 Apr;96(4):426-38. doi: 10.1113/expphysiol.2010.055780. Epub 2011 Jan 28.
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Development of electrocardiogram intervals during growth of FVB/N neonate mice.FVB/N新生小鼠生长过程中心电图间期的发育
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A coupled SYSTEM of intracellular Ca2+ clocks and surface membrane voltage clocks controls the timekeeping mechanism of the heart's pacemaker.细胞内 Ca2+ 时钟和细胞膜电压时钟的耦合系统控制着心脏起搏器的计时机制。
Circ Res. 2010 Mar 5;106(4):659-73. doi: 10.1161/CIRCRESAHA.109.206078.
8
The role of the funny current in pacemaker activity.有趣电流在起搏器活动中的作用。
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Cardiac T-type Ca(2+) channels in the heart.心脏中的 T 型钙通道。
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Age-dependent changes in Na current magnitude and TTX-sensitivity in the canine sinoatrial node.犬窦房结钠电流幅度和 TTX 敏感性的年龄依赖性变化。
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小鼠出生后心率增加和窦房结起博活动增强的机制。

The mechanism of increased postnatal heart rate and sinoatrial node pacemaker activity in mice.

机构信息

Department of Cell Physiology, Akita University Graduate School of Medicine, 1-1-1 Hondo, Akita 010-8543, Japan.

出版信息

J Physiol Sci. 2013 Mar;63(2):133-46. doi: 10.1007/s12576-012-0248-1. Epub 2013 Jan 4.

DOI:10.1007/s12576-012-0248-1
PMID:23288563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10717579/
Abstract

Heart rate (HR) of mammalian species changes postnatally, i.e., HR of large animals including humans decreases, while HR in small animals such as mice and rats increases. To clarify cellular mechanisms underlying the postnatal HR changes, we performed in vivo HR measurement and electrophysiological analysis on sinoatrial node (SAN) cells in mice. The in vivo HR was ~320 beats min(-1) (bpm) immediately after birth, and increased with age to ~690 bpm at postnatal day 14. Under blockage of autonomic nervous systems, HR remained constant until postnatal day 5 and then increased day by day. The spontaneous beating rate of SAN preparation showed a similar postnatal change. The density of the L-type Ca(2+) current (LCC) was smaller in neonatal SAN cells than in adult cells, accompanied by a positive shift of voltage-dependent activation. Thus, the postnatal increase in HR is caused by both the increased sympathetic influence and the intrinsic activity of SAN cells. The different conductance and kinetics of LCC may be involved in the postnatal increase in pacemaker activity.

摘要

哺乳动物的心率(HR)在出生后会发生变化,即包括人类在内的大型动物的 HR 降低,而小鼠和大鼠等小型动物的 HR 增加。为了阐明导致出生后 HR 变化的细胞机制,我们对小鼠的窦房结(SAN)细胞进行了体内 HR 测量和电生理分析。出生后立即,体内 HR 约为 320 次/分钟(bpm),并随年龄增长至出生后第 14 天增加至约 690 bpm。在阻断自主神经系统后,HR 直到出生后第 5 天保持不变,然后每天增加。SAN 制剂的自发搏动率也表现出类似的出生后变化。与成年细胞相比,新生 SAN 细胞中的 L 型钙(Ca2+)电流(LCC)密度较小,同时伴有电压依赖性激活的正偏移。因此,HR 的出生后增加是由交感神经影响的增加和 SAN 细胞的固有活动共同引起的。LCC 的不同电导和动力学可能参与了起搏活动的出生后增加。