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. 2020 Jul 9;5(13):e138505. doi: 10.1172/jci.insight.138505

Figure 2. Reduced vascular NO production blunted acetylcholine-induced vasorelaxation and enhanced AngII-mediated vasoconstriction in the EC-EP4–/– mice.

Figure 2

(A–C) The NO content in serum (A), aortas (B), and mesenteric arteries (C) of the EP4fl/fl and EC-EP4–/– mice. *P < 0.05, n = 7–8. (D and E) Vasodilatory response of the mesenteric arteries from the EP4fl/fl and EC-EP4–/– mice to acetylcholine (Ach) with (D) or without (E) preincubation of l-NAME. ***P < 0.001, n = 4. (F) Similar vasorelaxant response of the mesenteric arteries from the EP4fl/fl and EC-EP4–/– mice to SNP. n = 8. (G and H) Vasoconstrictive response of the mesenteric arteries to AngII with (G) or without (H) preincubation of l-NAME in the EP4fl/fl and EC-EP4–/– mice with 28-day exposure to chronic AngII infusion. ***P < 0.001, n = 4. Data are represented as mean ± SEM; 2-tailed Student’s t test for A–C; 2-way ANOVA tests for D–H.