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AIM: To characterize the electrophysiological and kinetic properties of Ca2+-activated chloride channel (CaCC) in cultured human umbilical vein endothelial cell line (HUVEC), and test the inhibitory effects of tetrandrine (Tet) on CaCC. METHODS: Ca2+-activated Cl- currents (ICl,Ca) were recorded by patch-clamp whole cell configurations. [Ca2+]i was measured via intracellular Fura-2 fluorescence intensities. RESULTS: ICl,Ca was activated by increasing [Ca2+]i via direct elevation of intracellular calcium. ICl,Ca showed an apparent outward rectification properties, and it was activated in a voltage- and calcium-dependent mode. Tet dose-dependently inhibited ICl,Ca, the IC50 was (5.2±0.4) μmol/L (n=8 cells). Tet suppressed both voltage-dependent and calcium-dependent activation of ICl,Ca. The activa- tion time constant was (326±12) ms [in the presence of 10 μmol/L Tet, compared to control (175±17) ms, at +100 mV], and Ca2+ concentration for half maximal activation was (387±61) nmol/L for Tet (compared to control (287±36) nmol/L. CONCLUSIONS: Tet effectively blocked ICl,Ca, and such effects might be due to its inhibitory effects on the activation process of Ca2+-activated chloride channel.
AIM: To characterize the electrophysiological and kinetic properties of Ca2 + -activated chloride channel (CaCC) in cultured human umbilical vein endothelial cell line (HUVEC), and test the inhibitory effects of tetrandrine (Tet) on CaCC. METHODS: Ca2 + RESULTS: ICl, Ca was activated by increasing [Ca2 +] i via direct elevation of intracellular calcium. (ICl, Ca) were recorded by patch-clamp whole cell configurations. [Ca2 +] i was measured via intracellular Fura- ICl, Ca showed an apparent outward rectification properties, and it was activated in a voltage- and calcium-dependent mode. Tet dose-dependently inhibited ICl, Ca, the IC50 was (5.2 ± 0.4) . Tet suppressed both voltage-dependent and calcium-dependent activation of IC1, Ca. The activa tion time constant was (326 ± 12) ms [in the presence of 10 μmol / L Tet, compared to control (175 ± 17) ms , at +100 mV], and Ca2 + concentration for half maximal activation was (387 ± 61) nmol / L for Tet (compared to control (287 ± 36) nmol / L. CONCLUSIONS: Tet block blocked ICl, Ca, and such effects might be due to its inhibitory effects on the activation process of Ca2 + -activated chloride channel.