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- W2766448249 abstract "Abstract Voltage-dependent inward currents responsible for the depolarizing phase of action potentials were characterized in smooth muscle cells of 4 th order arterioles in mouse skeletal muscle. Currents through L-type Ca 2+ channels were expected to be dominant; however, action potentials were not eliminated in nominally Ca 2+ -free bathing solution or by addition of L-type Ca 2+ channel blocker nifedipine (10 μM). Instead, Na + channel blocker tetrodotoxin (TTX, 1 μM) reduced the maximal velocity of the upstroke at low, but not at normal (2 mM), Ca 2+ in the bath. The magnitude of TTX-sensitive currents recorded with 140 mM Na + was about 20 pA/pF. TTX-sensitive currents decreased five-fold when Ca 2+ increased from 2 to 10 mM. The currents reduced three-fold in the presence of 10 mM caffeine, but remained unaltered by 1 mM of isobutylmethylxanthine (IBMX). In addition to L-type Ca 2+ currents (15 pA/pF in 20 mM Ca 2+ ), we also found Ca 2+ currents that are resistant to 10 μM nifedipine (5 pA/pF in 20 mM Ca 2+ ). Based on their biophysical properties, these Ca 2+ currents are likely to be through voltage-gated T-type Ca 2+ channels. Our results suggest that Na + and at least two types (T- and L-) of Ca 2+ voltage-gated channels contribute to depolarization of smooth muscle cells in skeletal muscle arterioles. Voltage-gated Na + channels appear to be under a tight control by Ca 2+ signaling." @default.
- W2766448249 created "2017-11-10" @default.
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- W2766448249 date "2017-11-01" @default.
- W2766448249 modified "2023-10-18" @default.
- W2766448249 title "Voltage-dependent inward currents in smooth muscle cells of skeletal muscle arterioles" @default.
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- W2766448249 doi "https://doi.org/10.1101/211540" @default.
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