SARCOLEMMAL NA+-CA-2+ EXCHANGE AND CA-2+-PUMP ACTIVITIES IN CARDIOMYOPATHIES DUE TO INTRACELLULAR CA-2+-OVERLOAD
SARCOLEMMAL NA+-CA-2+ EXCHANGE AND CA-2+-PUMP ACTIVITIES IN CARDIOMYOPATHIES DUE TO INTRACELLULAR CA-2+-OVERLOAD
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DOI：
10.1007/bf00242519
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发表时间：
1988-07-01
影响因子：
4.3
通讯作者：
BEAMISH, RE
中科院分区：
文献类型：
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作者：
DHALLA, NS;PANAGIA, V;BEAMISH, RE
为了确定心肌病心脏中 Na+-Ca2+ 交换和 Ca2+ 泵系统的缺陷，通过使用心肌病仓鼠 (UM-X7.1) 和注射儿茶酚胺诱发的心肌病，检查肌膜 Na+ 依赖性 Ca2+ 摄取、Na+ 诱导的 Ca2+ 释放、ATP 依赖性 Ca2+ 摄取和 Ca2+ 刺激的 ATPase 的活性。将异丙肾上腺素注入大鼠体内。遗传相关心肌病以及儿茶酚胺诱导的心肌病心脏的肌膜囊泡的 Na+ 依赖性 Ca2+ 摄取率、ATP 依赖性 Ca2+ 摄取率和 Ca2+ 刺激的 ATP 酶活性均降低，而 Na+ 诱导的 Ca2+ 释放没有任何变化。当用含 1.25 mM Ca2+ 的培养基灌注离体大鼠心脏 5 分钟，然后用不含 Ca2+ 的培养基灌注 5 分钟时，Ca2+ 悖论中也获得了类似的结果。尽管无 Ca2+ 灌注心脏再灌注 2 分钟会抑制肌膜 Ca2+ 泵活性，而 Na+ 诱导的 Ca2+ 释放没有任何变化，但 Na+ 依赖性 Ca2+ 摄取增加。这些结果表明，肌膜 Ca2+ 流出机制的改变可能在与细胞内 Ca2+ 超负荷的发展相关的心肌病中发挥重要作用。
In order to identify defects in Na+-Ca2+exchange and Ca2+-pump systems in cardiomyopathic hearts, the activities of sarcolemmal Na+-dependent Ca2+uptake, Na+-induced Ca2+release, ATP-dependent Ca2+uptake and Ca2+-stimulated ATPase were examined by employing cardiomyopathic hamsters (UM-X7.1) and catecholamine-induced cardiomyopathy produced by injecting isoproterenol into rats. The rates of Na+-dependent Ca2+uptake, ATP-dependent Ca2+uptake and Ca2+-stimulated ATPase activities of sarcolemmal vesicles from genetically-linked cardiomyopathic as well as catecholamine-induced cardiomyopathic hearts were decreased without any changes in Na+-induced Ca2+-release. Similar results were obtained in Ca2+-paradox when isolated rat hearts were perfused for 5 min with a medium containing 1.25 mM Ca2+following a 5 min perfusion with Ca2+-free medium. Although a 2 min reperfusion of the Ca2+-free perfused hearts depressed sarcolemmal Ca2+-pump activities without any changes in Na+-induced Ca2+-release, Na+-dependent Ca2+uptake was increased. These results indicate that alterations in the sarcolemmal Ca2+-efflux mechanisms may play an important role in cardiomyopathies associated with the development of intracellular Ca2+overload.