Erratum: Zinc deficiency induces hypertension by promoting renal Na⁺reabsorption (American Journal of Physiology - Renal Physiology (2019) 316 (F646-F653) DOI: 10.1152/ajprenal.00487.2018)

In this article, in terms of experimental procedures, mice were group housed for metabolic cage studies; for the RESULTS, there are some data for urinary values where the units have to be corrected. These changes did not alter any of the conclusions of the study. Corrections are detailed below. In EXPERIMENTAL DESIGN, BP Regulation, Na excretion, the paragraph should read as follows: Metabolic cage studies were performed to measure urinary Naexcretion. Mice were group housed (5 mice/cage). After a 24-h acclimation period, 24-h urine samples were collected. Na was measured using a Medica EasyLyte Plus Na K Cl analyzer. Total Na excretion was calculated by multiplying Na concentration by total urine output/24 h/cage. In RESULTS, ZnD Causes Increased BP and Dysregulated Renal Na Transport, the second paragraph should read as follows: Concurrently, 24-h urinary Na excretion was measured (Fig. 1D). BP changes were accompanied by corresponding changes in urinary Na excretion. During the pressor phases, urinary Na levels were significantly decreased in ZnD mice at week 1 (836.3 87.76 vs. 1,198.4 62.52 mol) and week 6 (937.0 53.54 vs. 1,338.0 144.40 mol) compared with ZnA mice. However, during the normotensive phase, urinary Na levels were not statistically different at week 3 (1,092.4 76.36 vs. 1,140.1 84.35 mol). Like urinary Na excretion, the amount of Cl excreted during the pressor phases was less in ZnD mice (863.9- 64.30 vs. 1,135.7- 59.84 mol at week 1 and 950.7- 49.34 vs. 1,400.5 180.8mol at week 6), while urinary Cl levels were unaltered during the normotensive phase (1,078.2 66.55 vs. 1,167.5 90.53 mol at week 3). However, urinary K excretion was reduced during all phases (616.0 57.43 vs. 824.4 38.99mol at week 1, 625.6 46.46 vs. 826.7-49.61 mol at week 3, and 593.9 19.29 vs. 963.3-89.80 mol at week 6). Together, these results indicate that ZnD-induced BP increases are accompanied by reduced renal Na, Cl, and K excretion. In RESULTS, NCC Mediates ZnD-Induced Hypertension, first paragraph, the final sentences should read as follows: Furthermore, urinary Na levels were elevated in response to HCTZ administration compared with vehicle-treated ZnD mice (1,227.7 29.58 vs. 1,032.5 30.39 mol). This finding indicates an increase in NCC activity. In RESULTS, Zn2 Regulates BP and NCC, first paragraph, the final sentence should read as follows: Furthermore, this reduction in BP was accompanied by elevated urinary Na levels (1,280.9 31.92 vs. 937.0 75.72 mol). The corrected values are shown in Fig.