Abstract
Although many electrophysiological properties of the cardiac and smooth muscle L-type calcium channels (CC) are identical, they differ in their hormonal regulation, β -adrenergic stimulation increases the calcium inward current by cAMP-dependent phosphorylation of the CC or a closely associated protein in cardiac myocytes [1], but not in smooth muscle cells [2]. Cloning of the cDNA of both channels showed that they are composed of at least three proteins, the channel containing α1 subunit and two auxiliary subunits, the β and α2/γ [3]. The α1 subunit, a product of the class C gene, has several splice variants, containing identical putative phosphorylation sites. The cardiac and smooth muscle CC complexes presumably contain different β subunits [4] and an identical α2/γ protein. The cloned α1 subunit has been expressed stably or transiently, alone or in combination with the α2/γ subunit and different β subunits, in CHO and HEK 293 cells. In each system, the α1 subunit codes for a functional L-type CC which has many properties of the native cardiac or smooth muscle channel [5]. Recent reports show that barium currents (IBa) of the stable expressed α1c subunit increased following treatment with dBcAMP [6], the catalytic subunit of cAMP kinase [7] or forskolin [8]. Dialysis of the CHO cells stably expressing the cardiac (α1Ca) or smooth muscle (βlcb) α1 subunit with the PKI inhibitor peptide 5–25 (1 mM), the pure catalytic subunit of cAMP kinase (cAMP kinase, 25 μM), or a combination of okadaic acid (1 μM) and cAMP kinase, had no significant effect on IBa.
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© 1995 Birkhäuser Verlag Basel/Switzerland
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Godfraind, T., Atkinson, J. (1995). Novel Aspects of the Pharmacology of Calcium Channel Modulators. In: Cuello, A.C., Collier, B. (eds) Pharmacological Sciences: Perspectives for Research and Therapy in the Late 1990s. Birkhäuser Basel. https://doi.org/10.1007/978-3-0348-7218-8_11
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DOI: https://doi.org/10.1007/978-3-0348-7218-8_11
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