Abstract
This review analyzes the structure and regulation mechanisms of voltage-dependent L-type Ca(2+) channel in the heart. L-type Ca(2+) channels in the heart are composed of four different polypeptide subunits, and the pore-forming subunit alpha(1) is the most important part of the channel. In cardiac myocytes, Ca(2+) enter cell cytoplasm from extracellular space mainly through L-type Ca(2+) channels; these channels are very important system in heart Ca(2+) uptake regulation. L-type Ca(2+) channels are responsible for the activation of sarcoplasmic reticulum channels (RyR2) and force of muscle contraction generation in heart; hence, activity of the heart depends on L-type Ca(2+) channels. Phosphorylation of channel-forming subunits by different kinases is one of the most important ways to change the activity of L-type Ca(2+) channel. Additionally, the activity of L-type Ca(2+) channels depends on Ca(2+) concentration in cytoplasm. Ca(2+) current in cardiac cells can facilitate, and this process is regulated by phosphorylation of L-type Ca(2+) channels and intracellular Ca(2+) concentration. Disturbances in cellular Ca(2+) transport and regulation of L-type Ca(2+) channels are directly related to heart diseases, life quality, and life span.
Highlights
The stimulation of b-adrenergic receptors and subsequent activation of PKA, which results in modulation of L-type Ca2+ channel, is the best-investigated pathway of Ca2+ channel regulation
It is showed that M2 muscarinic receptors can suppress ICa of cardiac cells by activation of phosphatases or by changing cGMP-dependent phosphodiesterase activity in participation of NO [28]
In the phosphorylation of membrane targets, specific anchoring proteins referred to as RACKs are playing an important role; protein kinase C (PKC) interacts with RACKs in an isoform-specific manner [14, 29]
Summary
The stimulation of b-adrenergic receptors and subsequent activation of PKA, which results in modulation of L-type Ca2+ channel, is the best-investigated pathway of Ca2+ channel regulation. It is showed that M2 muscarinic receptors can suppress ICa of cardiac cells by activation of phosphatases or by changing cGMP-dependent phosphodiesterase activity in participation of NO [28].
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