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. 2022 Sep 29;11(19):e026581. doi: 10.1161/JAHA.122.026581

Figure 5. Kidney epithelial cells‐specific EP4 deletion leads to augmented natriuretic response to amiloride during Ang II‐HTN.

Figure 5

Mice received Ang II infusion at 1000 ng/kg per min. On day 11 of Ang II infusion, 24 hours of urine was collected, and on day 12 of Ang II infusion, mice were given amiloride 4 mg/kg (intraperitoneal.) and 24 hours of urine was collected immediately after the amiloride injection. Following amiloride treatment, the urine sodium excretion significantly increased in both Control and KEKO mice (A and B). However, the total urine sodium excretion (A and B) and the change in urine sodium excretion compared with baseline (C) were significantly higher in KEKOs. Data are expressed as raw value (A), mean±SEM (B), or median with interquartile range (C); (B) is analyzed by 2‐way ANOVA (factors: genotype and treatment) with Sidak multiple comparisons tests; (C) is analyzed by Mann–Whitney test; *P<0.05, **P<0.01; ***P<0.001; effect size: medium for (B) Control baseline vs KEKO baseline, large for all other significant comparisons; n=4/group. Ang II‐HTN indicates angiotensin II‐dependent hypertension; BP, blood pressure; EP4, E‐prostanoid receptor 4; and KEKO, kidney epithelial cell‐specific EP4 receptor knockout.