Calycosin and Formononetin Induce Endothelium-Dependent Vasodilation by the Activation of Large-Conductance Ca²⁺-Activated K⁺ Channels (BK_Ca)

Figure 5

Calycosin increased outward currents in HUVEC through channel. (a) Current-voltage () relationship in response to calycosin (1–100 μM). (b) Dose-response curve for whole cell recording of currents at +100 mV with different concentrations of calycosin (10 nM–100 μM). (c, d) Representative trace of currents that were recorded in response to calycosin in the absence or presence of (c) TEACl (1 mM) or (d) IbTX (200 nM). (e, f) Whole cell recording of currents at +100 mV in response to calycosin (100 μM) in the presence of (e) apamin (200 nM), IbTX (200 nM), ChTX (200 nM), or TEACl (1 mM; versus control; and versus calycosin-treated cells), or (f) with different as indicated ( and versus calycosin-treated cells with free ). Data were shown as mean ± SEM. ChTX, charybdotoxin; IbTX, iberiotoxin; TEACl, tetraethylammonium chloride.

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