Table of Contents Author Guidelines Submit a Manuscript
BioMed Research International
Volume 2015, Article ID 780814, 13 pages
Research Article

Nitric Oxide Protects L-Type Calcium Channel of Cardiomyocyte during Long-Term Isoproterenol Stimulation in Tail-Suspended Rats

Department of Aerospace Physiology, Fourth Military Medical University, No. 169 Changlexi Road, Xi’an 710032, China

Received 15 April 2015; Accepted 30 May 2015

Academic Editor: Jun Ren

Copyright © 2015 Zhi-Jie Yue et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 () in the SUS group was less than that in the CON group. The maximal 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 to 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximal in SUS group to similar extent of CON group after 50 min of ISO treatment. Long-term ISO stimulation also changed steady-state activation (), inactivation (), and recovery () 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.