Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy

Enhanced sarcolemmal Ca2+ efflux reduces sarcoplasmic reticulum Ca2+ content and systolic Ca2+ in cardiac hypertrophy
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DOI:
10.1016/j.cardiores.2004.01.038
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发表时间:
2004-06-01
影响因子:
10.8
通讯作者:
Trafford, AW
Trafford, AW
中科院分区:
医学1区
文献类型:
--
作者:
Díaz, ME;Graham, HK;Trafford, AW

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目的:最近的工作已经确定了心脏疾病状态下收缩Ca2+瞬态的减少。本研究的目的是确定在分离的心肌细胞中细胞内钙稳态扰动的机制,并确定这种变化是否可以定量地解释收缩Ca2+瞬态减少。方法:采用主动脉缩窄法诱导成年雪貂左心室肥厚(LVH)。在单个左心室心肌细胞中测量细胞内Ca2+调节,肌层Ca2+通量和SR功能的变化。结果:心肌肥厚与动作电位持续时间增加29%相关(APD(90));收缩期Ca2+瞬态的振幅降低48%,衰减速率减慢19%;在给定的[Ca2+]变化(i)下,SR Ca2+含量降低20%,向内Na+-Ca2+交换电流增加36%
Objective: Recent work has identified reductions in the systolic Ca2+ transient in cardiac disease states. The aim of the present study was to identify the mechanisms responsible for perturbations of intracellular calcium homeostasis in isolated cardiac myocytes and determine if such changes can quantitatively explain the reduced systolic Ca2+ transient. Methods: Left ventricular hypertrophy (LVH) was induced by aortic coarctation in adult ferrets. Changes in intracellular Ca2+ regulation, sarcolemmal Ca2+ fluxes and SR function were measured in single left ventricular cardiac myocytes. Results: Cardiac hypertrophy was associated with a 29% increase in action potential duration (APD(90)); a 48% reduction in the amplitude of and 19% slowing in the rate of decay of the systolic Ca2+ transient; a 20% decrease in SR Ca2+ content and a 36% increase in inward Na+-Ca2+ exchange current for a given change in [Ca2+](i) (all P