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. 2021 Jun 24;12:692719. doi: 10.3389/fphys.2021.692719

Figure 5.

Figure 5

AITC (100 μM) enhancement of SBCs is mediated by the release of prostaglandins (PG) and not by the release of substance P (SP). (A) AITC enhances SBCs and this effect is reversed to inhibition by pretreatment with indomethacin (INDO, 500 nM) (B) which is in turn reversed by a wash (gap in record represents 24 min). (C) Prostaglandin E2 (PGE2, 500 nM) mimicks the excitatory effect of AITC. (D) SP (1 μM) enhances SBCs; however, this effect is not blocked by INDO (E) but is blocked by a cocktail of neurokinin receptor 1, 2, and 3 antagonists (1 μM each) which does not block the excitatory effect of AITC (F). (G) Effects of agonists and antagonists shown in (A–F) are summarized as % change in SBC AUC compared to basal activity, data were obtained from single experiments with either a pristine agonist or an antagonist followed by an agonist (H). After indomethacin (INDO) treatment AITC reduces SBC and this effect is reversed by BIBN as shown in Figure 4E. Statistics were performed on raw numbers: (G,H), 2-tailed t-test, *P < 0.05 and **P < 0.001, and a two-way ANOVA with Bonferroni multiple comparisons post-hoc tests were performed to compare the antagonist effects (brackets), #P < 0.05; n, number of strips.