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pubmed:abstractText |
The L-type calcium channel plays a pivotal role in the regulation of a wide range of cellular processes, including membrane excitability, Ca(2+) homeostasis, protein phosphorylation, and gene regulation. Alterations in the density or function of the L-type calcium channel have been implicated in a variety of cardiovascular diseases. Our previous study found that acute restraint stress could cause an enhancement of the L-type calcium current (I (Ca-L))(,) which correlated with an up-regulation of activation characters of the calcium channel. In this study, we observed the change of I (Ca-L) in rat ventricular myocytes under chronic restraint stress using the whole-cell patch-clamp technique and further explored its modulation mechanisms. The results showed that chronic restraint stress could also enhance I (Ca-L), but increased I (Ca-L) was not accompanied by an alteration of the characteristics of activation and inactivation of the L-type calcium channel. Furthermore, results from reverse-transcription polymerase chain reaction and Northern blot showed that the abundance of alpha(1c) subunit messenger RNA of the L-type calcium channel in the ventricle was increased significantly after chronic stress, and Western blot analysis revealed the amount of alpha(1c) subunit protein also was elevated. These results suggest that the L-type calcium channel is involved in stress-induced cardiomyocyte injury, and the up-regulated expression of the L-type calcium channel alpha(1c) subunit might contribute to the I (Ca-L) change under chronic stress, which is different from the regulation mechanism of acute restraint stress that mostly relates to an alteration in protein kinase A-dependent channel activation. Thus, it would provide a new insight into the mechanism of cardiomyocyte injury induced by stress.
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