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. 2019 May 28;9:7932. doi: 10.1038/s41598-019-44333-w

Figure 2.

Figure 2

Time course of the capsaicin-initiated inhibition of the ACh-induced NO-dependent vasodilator component. The experimental protocol of the results shown in A, B and C is depicted on the top of the figure. (A) Relaxation induced by 100 nM ACh in KCl-contracted mesenteric arteries in control conditions and 15 or 60 min after treatment with capsaicin (1 µM) or its vehicle for 20 min. ACh was applied in the presence of 10 µM indomethacin to prevent the interference of prostaglandins in the response. (B) NO production induced by successive ACh (100 nM) stimulations along the time in mesenteric arterial beds treated with capsaicin or the vehicle. (C) Relaxation induced by 300 nM SNAP, a NO donor, in KCl-contracted mesenteric arteries before (control) or 15 or 60 min after treatment with capsaicin or its vehicle. Values are means ± SEM. *P < 0.05 vs control by one-way ANOVA plus Dunnett post hoc test.