*2.3. B. monnieri Compounds and Ca2*<sup>+</sup> *Influx*

Voltage-operated Ca2<sup>+</sup> channels (VOCCs) were activated by depolarising denuded vessels with 80 mM K<sup>+</sup> in Ca2<sup>+</sup>-free Krebs' solution. Then vascular contraction elicited by CaCl2 accumulatively added at increasing concentrations (0.01–10 mM). In the same vessel, the protocol was repeated by pre-incubation with 10 μM *B. monnieri* compounds for 15 min and these CaCl2-induced contractions were inhibited and seen as a rightward shift of the plots and reduced Emax from control (Figure 3).

**Figure 3.** CaCl2-induced contractions of denuded mesenteric arteries pre-incubated in high K<sup>+</sup>, Ca2+-free media in the conditions of pre-incubation with DMSO (negative control), 10 μM bacopaside I, 10 μM luteolin, 10 μM apigenin, and 1 μM nicardipine (positive control). *Y*-axis, % contraction compared to the contraction achieved with the highest Ca2<sup>+</sup> concentration during the initial run without a *B. monnieri* compound in the same vessel. Values are mean ± SEM of 4–6 individual arteries. \*\* *p* < 0.01 each of the active compounds compared to DMSO using two-way ANOVA (n = 4–6).

The maximum contraction (Emax) of control, bacopaside I, luteolin and apigenin were 100 ± 1.3, 81.9 <sup>±</sup> 1.7, 72.0 <sup>±</sup> 6.7 and 40.2 <sup>±</sup> 3.5%, respectively. Positive control, L-type Ca2<sup>+</sup>-channel blocker, nicardipine (1 μM) completely abolished this CaCl2-induced vasoconstriction (Figure 3).
