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Basal dephosphorylation controls slow gating of L‐type Ca 2+ channels in human vascular smooth muscle
Author(s) -
Groschner Klaus,
Schuhmann Klaus,
Baumgartner Werner,
Pastushenko Vassili,
Schindler Hansgeorg,
Romanin Christoph
Publication year - 1995
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(95)01012-4
Subject(s) - dephosphorylation , vascular smooth muscle , phosphatase , gating , chemistry , phosphorylation , umbilical vein , smooth muscle , biochemistry , biophysics , microbiology and biotechnology , biology , endocrinology , in vitro
The role of cellular phosphatase activity in regulation of smooth muscle L‐type Ca 2+ channels was investigated using tautomycin, a potent and specific inhibitor of serin/threonin phosphatases type 1 and 2A. Tautomycin (1–100 nM) inhibited Ca 2+ channel activity in smooth muscle cells isolated from human umbilical vein. Tautomycin‐induced inhibition of Ca 2+ channel activity was due to a reduction of channel availability which originated mainly from prolongation of the lifetime of unavailable states of the channel. Pretreatment of smooth muscle cells with the protein kinase inhibitor H‐7 (10 μM) prevented the inhibitory effect of tautomycin. Our results suggest modulation of slow gating between available and unavailable states as a mechanism of phosphorylation‐dependent down‐regulation of Ca 2+ channels in vascular smooth muscle.