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. 2019 Apr 4;116(17):8457–8462. doi: 10.1073/pnas.1902119116

Fig. 6.

Fig. 6.

VSMC-specific EP4 gene deletion causes hypertension. (A) Mean arterial blood pressure (MAP) levels in WT and VSMC-EP4−/− mice. Anesthetized EP4f/f and VSMC-EP4−/− mice were measured via the carotid arterial catheterization. n = 32–69; **P < 0.01 vs. EP4f/f. (B) Systolic blood pressure in EP4f/f and VSMC-EP4−/− mice at the baseline and in response to chronic AngII infusion. Blood pressure was monitored via tail cuff every 7 d over 3 wk. n = 9–26; *P < 0.05 vs. EP4f/f+AngII. (C) AngII-evoked vasoconstriction of mesenteric arterial rings from EP4f/f and EP4−/− mice. The rings were pretreated with N(ω)-nitro-l-arginine methyl ester (l-NAME, 100 μM) and then challenged with various doses of AngII. n = 10; *P < 0.05; **P < 0.01 vs. EP4f/f. (D) Representative images of AngII-elicited intracellular Ca2+ increase in VSMCs. VSMCs were pretreated with or without the EP4 antagonist MF498. ▼ represents Ca2+ fluorescence images at the baseline. * indicates images at the peak of induction. (E) The ratio of peak-to-basal change (ΔF/F0) in Fluo-4 acetoxymethyl fluorescence intensity in VSMCs treated with or without MF498. n = 7–12; *P < 0.05 vs. control.