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. 2022 Jun 8;79(8):1668–1679. doi: 10.1161/HYPERTENSIONAHA.121.18791

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© 2022 The Authors.

Hypertension is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 4. — Gastrin inhibits Na+/H+ exchanger 3 (NHE3) expression via NHERF1 and NHERF2-mediated protein trafficking. A, Expressions of NHE3, NHERF1, NHERF2, NHERF3, ezrin, and IRBIT in intestinal brush border membranes of knockout (KO) mice and wild-type (WT) mice fed normal (N) or high (H) salt diet (n=4/group, *P<0.01 vs Cckbr^fl/fl WT, 1-way ANOVA, Holm-Sidak test). B, Expressions of NHE3, NHERF1, NHERF2, NHERF3, ezrin, and IRBIT in the intestinal brush border membrane of Dahl salt-sensitive (DSS) rats. Villin was used as an internal marker of intestinal epithelial cells (*P<0.05 vs DSS control [0.49% NaCl], #P<0.05 vs DSS + high salt [HS, 8% NaCl], 1-way ANOVA, Tukey test). C and D, AAV-NHERF1 and AAV-NHERF2 plasmids impair the effectiveness of the gastrin-SiO₂ microspheres in ameliorating the increase in systolic blood pressure (BP) and impairing the increase in urine Na concentration in DSS rats fed HS diet (*P<0.05 vs others, # vs DSS + others, 1-way ANOVA, Tukey test).