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. Author manuscript; available in PMC: 2022 Apr 1.
Published in final edited form as: Hypertension. 2021 Mar 1;77(4):1399–1411. doi: 10.1161/HYPERTENSIONAHA.120.16518

Figure 2. Vasodilation: Role of Cyclooxygenase.

Figure 2.

A) Schematic representation of the cyclooxygenase (COX)/prostaglandin E2 (PGE2)/E-prostanoid receptors pathway and pharmacological agents targeting different components of the pathway. PTGES1-3, prostaglandin E synthase 1-3; HPGD, 15-Hydroxyprostaglandin Dehydrogenase. B) Vasoconstriction was measured in carotid artery in response to U46619 (60 nmol/L) preincubated in the presence or absence of the non-specific COX inhibitor indomethacin (Indo, 30 min pre-incubation at 10 μmol/L)(n=8-11 as indicated). C-D) Effects of indomethacin on ACh-induced and SNP-induced vasodilation in the carotid artery (C, n=6-9; D, n=7-8). Curves with diamonds denote indomethacin-treated vessel segments. Curves with filled circles (chow) and squares (HSD) represent vehicle-treated vessel segments. Data are plotted as mean ± SEM. Two-way ANOVA RM was performed to determine whether two curves there different (main-group effect, denoted by statistical symbols on the right of the curve). †p<0.05, S-P467L chow diet vs NT chow diet; *p<0.05, S-P467L HSD vs NT HSD; #p<0.05, Indomethacin-treated vs vehicle-treated. Dose response curves were analyzed by nonlinear regression to generate EC50 and Emax values listed in the insets.