Key result
PKC inhibition reduces LVGC conductance by ~65% in wild-type myocytes but less in NCX1-deficient cells.
Why the study?
The regulation of L-type voltage-gated Ca2+ channels by protein kinase C in arterial smooth muscle cells with smooth muscle-specific Na+/Ca2+ exchanger knockout was unclear.
Population
Arterial smooth muscle cells from wild-type and NCX1(SM-/-) mice
Comparison
PKC activators and inhibitors effects in WT vs NCX1(SM-/-) myocytes
Design
Preclinical experimental study using pharmacological modulators
Authors
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PKC-Ca2+ channel regulation partly depends on NCX1 in murine myocytes; leaves open relevance to human Ca2+-driven arrhythmias or HF.
Absolute Event Rate: 37% vs 65%
In arterial smooth muscle cells, reduced Ca2+ entry via NCX1 lowers cytosolic Ca2+, which reduces PKC activation and subsequently lowers L-type voltage-gated Ca2+ channel activation.
Ren et al. (2010) studied this question. Smooth muscle-specific Na+/Ca2+ exchanger type-1 knockout (NCX1(SM-/-)) vs. Wild-type (WT) mice was evaluated on Decrease in LVGC conductance with PKC inhibition (PKC 19-31). Inhibition of PKC decreased L-type voltage-gated Ca2+ channel conductance by 65% in wild-type myocytes but by only 37% in NCX1(SM-/-) myocytes.
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