Activation of calcium release assessed by calcium release-induced inactivation of calcium current in rat cardiac myocytes.

Activation of calcium release assessed by calcium release-induced inactivation of calcium current in rat cardiac myocytes.
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通过大鼠心肌细胞中钙释放诱导的钙电流失活来评估钙释放的激活。

DOI:
10.1152/ajpcell.00272.2003
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发表时间:
2004
期刊:
American journal of physiology. Cell physiology
影响因子:
--
通讯作者:
Zahradník,Ivan
Zahradník,Ivan
中科院分区:
--
文献类型:
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作者:
Zahradníková,Alexandra;Kubalová,Zuzana;Pavelková,Jana;Györke,Sándor;Zahradník,Ivan

文献摘要

相似文献

In mammalian cardiac myocytes, calcium released into the dyadic space rapidly inactivates calcium current (ICa). We used this Ca2+release-dependent inactivation (RDI) ofICaas a local probe of sarcoplasmic reticulum Ca2+release activation. In whole cell patch-clamped rat ventricular myocytes, Ca2+entry induced by short prepulses from —50 mV to positive voltages caused suppression of peakICaduring a test pulse. The negative correlation between peakICasuppression andICainactivation during the test pulse indicated that RDI evoked by the prepulse affected only calcium channels in those dyads in which calcium release was activated. Ca2+ions injected during the prepulse and during the subsequent tail current suppressed peakICain the test pulse to a different extent. Quantitative analysis indicated that equal Ca2+charge was 3.5 times less effective in inducing release when entering during the prepulse than when entering during the tail. Tail Ca2+charge injected by the first voltage-dependent calcium channel (DHPR) openings was three times less effective than that injected by DHPR reopenings. These findings suggest that calcium release activation can be profoundly influenced by the recent history of L-type Ca2+channel activity due to potentiation of ryanodine receptors (RyRs) by previous calcium influx. This conclusion was confirmed at the level of single RyRs in planar lipid bilayers: using flash photolysis of the calcium cage NP-EGTA to generate two sequential calcium stimuli, we showed that RyR activation in response to the second stimulus was four times higher than that in response to the first stimulus.