Figure 3.

(A) Summary data showing that the OA-NO₂ inhibitory response is not blocked by a combination of a TRPV1 (diarylpiperazine, DP) and a TRPA1 antagonist (HC3; n = 16) or the TRPC antagonist (La³⁺, 50 μM; n = 9). (B,C) Summary data showing that DP and HC3 suppress the effects of CAPS (n = 12) and AITC (n = 16), respectively. (D) Summary data showing the time course of the inhibitory effect of OAG (n = 10–12) and the block of this effect by La³⁺ (50 μM; n = 6), 45 min after application of OAG. (E) Effect of various antagonists on SBC AUC shown as % change from control SBC activity before treatment. Neurokinin receptor antagonists (NK Antag), a combination of three antagonists subtypes (1, 2 and 3: SR 140333, SR 48968 and SR 142801, respectively, 1 μM of each drug); BIBN (25 μM, CGRP receptor antagonist), indomethacin (INDO, 500 nM, COX inhibitor), concentrations of TTX, La³⁺, DP, and HC3 are the same as those indicated in Figure 2. Data was obtained from single experiments with either a pristine agonist or an antagonist followed by an agonist and graphs are presented as % change in SBC area under the curve (AUC) compared to basal activity. Statistics were performed on raw numbers: (A–C) 2-tailed t-test, *P < 0.05 and **P < 0.001, and a two-way ANOVA with Bonferroni multiple comparisons post-hoc tests (brackets), ^#P < 0.05; (D) one-way ANOVA with Dunnett's multiple comparison post-hoc test (OAG; ⁺P < 0.05) and two-way ANOVA (bracket) with Bonferroni multiple comparisons post-hoc test (La³⁺; ^#P < 0.05); (E) 2-tailed t-test, *P < 0.05, compared with basal activity; n, number of strips].