nitric oxide protects l-type calcium channel of cardiomyocyte during long-term isoproterenol stimulation in tail-suspended rats

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ID: 194309
2015
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Abstract
The aim of this study was to investigate the effects of nitric oxide (NO) and reactive oxygen species (ROS) on L-type calcium channel (LTCC) gating properties of cardiomyocytes during long-term isoproterenol (ISO) stimulation. Expression and activity of nNOS as well as S-nitrosylation of LTCC α1C subunit significantly decreased in the myocardium of SUS rats. Long-term ISO stimulation increased ROS in cardiomyocytes of SUS rats. ISO-enhanced calcium current (ICa,L) in the SUS group was less than that in the CON group. The maximal ICa,L decreased to about 80% or 60% of initial value at the 50th minute of ISO treatment in CON or SUS group, respectively. Specific inhibitor NAAN of nNOS reduced maximal ICa,L to 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximal ICa,L in SUS group to similar extent of CON group after 50 min of ISO treatment. Long-term ISO stimulation also changed steady-state activation (P<0.01), inactivation (P<0.01), and recovery (P<0.05) characteristics of LTCC in SUS group. In conclusion, NO-induced S-nitrosylation of LTCC α1C subunit may competitively prevent oxidation from ROS at the same sites. Furthermore, LTCC can be protected by NO during long-term ISO stimulation.
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yue2015biomednitric Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Zhi-Jie Yue;Peng-Tao Xu;Bo Jiao;Hui Chang;Zhen Song;Man-Jiang Xie;Zhi-Bin Yu
Journal spectrochimica acta - part a: molecular and biomolecular spectroscopy
Year 2015
DOI
10.1155/2015/780814
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