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- W2084713627 abstract "L-type calcium channels are modulated in different fashions by Ca2+ (Ca2+ dependent inactivation, Ca2+ dependent facilitation), cytosolic proteins (CAM, CAMKII, PKA, PKC, etc) and voltage (voltage dependent inactivation). Here we describe a novel modulation of Ca2+ channel exerted by pressure/flow (PF) forces where 35-60% inhibition of IBa occurs when cells were exposed to 30 cm of PF forces. Only brief periods (300ms) of high PF applications were required to activate the response, but the effect was reversible and had a latency of ∼500-700 ms. Similar data was obtained in HEK cells expressing all the recombinant subunits of Ca2+ channel. To determine the mechanism underlying the PF effect, the current through the channel was measured in cells treated with 10µM of thapsigargin, or IP3R blocker APB-2 (10µM), or mitochondrial protonophore, FCCP + oligomycin, or high concentrations of BAPTA. We found no significant difference in effectiveness of PF pulses to inhibit IBa, or ICa in cell exposed to, thapsigargin, APB-2, FCCP, BAPTA or a mixed cocktail of them. We concluded that native Ca2+ channel of rat ventricle myocytes or recombinant human variants of L-type Ca2+ expressed in HEK cells can be modulated by PF forces. This mechanism may represent a different physiological regulation of calcium channels in the heart and blood vessels." @default.
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- W2084713627 date "2011-02-01" @default.
- W2084713627 modified "2023-10-16" @default.
- W2084713627 title "Mechanical Induced Inhibition of L-Type Calcium Channels" @default.
- W2084713627 doi "https://doi.org/10.1016/j.bpj.2010.12.3303" @default.
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