The concept of cardiac L-type calcium channel regulation via signal transduction processes and cAMP-dependent phosphorylation has become more elaborate over the past decade.
Provides a comprehensive review of the signal transduction and phosphorylation mechanisms regulating cardiac L-type calcium channels.
Voltage-dependent Ca2+ channels play a major role in the electromechanical coupling of cardiac cells. During the plateau phase Ca2+ entry induces a Ca2+ -dependent Ca2+ release from the sarcoplasmic reticulum and con sequently the initiation of contraction (for review see 41). Voltage-dependent Ca2+ channels are also involved in the spontaneous impulse generation as well as in the duration of the action potentials and hence in refractoriness. Ca2+ channels are also the target of various hormones and neurotransmitters. In an Annual Review of Physiology that appeared ten years ago, Reuter (112) suggested a hypothetical scheme for the �-adrenergic control of Ca2+ chan nels by cAMP-dependent phosphorylation, but direct experimental evidence for this was still missing (further reviews see 90, 125, 133, 134). In the subsequent decade the concept of regulation via the signal transduction process and phosphorylation became more elaborate by analysis of the
Trautwein et al. (Mon,) conducted a review in Cardiac L-Type Calcium Current regulation. The concept of cardiac L-type calcium channel regulation via signal transduction processes and cAMP-dependent phosphorylation has become more elaborate over the past decade.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: