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. 2019 Jul 25;24(15):2700. doi: 10.3390/molecules24152700

Figure 4.

Figure 4

Endothelium-dependent mechanism of the Calafate extract and anthocyanin vasodilation; endothelial nitric oxide synthase enzyme (eNOS) participation. (A) The vasodilatation elicited by 10 µg/mL extract (n = 10) or 100 nM of delphinidin-3-glucoside (D3G, n = 6), petunidin-3-glucoside (P3G, n = 6), malvidin-3-glucoside (M3G, n = 4), or acetylcholine (ACh, n = 19) perfused in intact mesenteries or by the same mesentery devoid of endothelium (-). In parallel, separate protocols evaluated the role of eNOS activity after enzyme blockade following tissue perfusion with 150 µM L-NNA. Vasorelaxations were normalized by the 1 µM ACh-induced vasodilation. Columns denote the mean values, bars the SEM. *, p < 0.05, **, p < 0.01, ***, p < 0.001 (B) Representative tracings of the vasodilatation elicited by 10 µg/mL Calafate extract before (control) and following eNOS inhibition with L-NNA. Note that after L-NNA treatment, the concentration of NA was reduced to 20 µM, because of tissue sensitization.