CORRIGENDUM.

Abstract

CorrigendumCORRIGENDUMPublished Online:08 Jul 2019https://doi.org/10.1152/ajprenal.zh2-8726-corr.2019Original articleMoreSectionsPDF (76 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Williams CR, Mistry M, Cheriyan AM, Williams JM, Naraine MK, Ellis CL, Mallick R, Mistry AC, Gooch JL, Ko B, Cai H, Hoover RS. Zinc deficiency induces hypertension by promoting renal Na+ reabsorption. Am J Physiol Renal Physiol 316: F646–F653, 2019. First published January 16, 2019; 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 Na+ excretion. 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 µmol) and week 6 (937.0 ± 53.54 vs. 1,338.0 ± 144.40 µmol) 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 µmol). 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 µmol at week 1 and 950.7 ± 49.34 vs. 1,400.5 ± 180.8 µmol at week 6), while urinary Cl− levels were unaltered during the normotensive phase (1,078.2 ± 66.55 vs. 1,167.5 ± 90.53 µmol at week 3). However, urinary K+ excretion was reduced during all phases (616.0 ± 57.43 vs. 824.4 ± 38.99 µmol at week 1, 625.6 ± 46.46 vs. 826.7 ± 49.61 µmol at week 3, and 593.9 ± 19.29 vs. 963.3 ± 89.80 µmol at week 6). Together, these results indicate that ZnD-induced BP increases are accompanied by reduced renal Na+, Cl−, and K+ excretion.Download figureDownload PowerPointIn 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 µmol). 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 µmol).The corrected values are shown in Fig. 1D, below:The corrected values are also shown in Fig. 2, B and F, below:Download figureDownload PowerPointThis article has no references to display. Download PDF Previous Back to Top FiguresReferencesRelatedInformation Related ArticlesZinc deficiency induces hypertension by promoting renal Na+ reabsorption 21 Mar 2019American Journal of Physiology-Renal Physiology More from this issue > Volume 317Issue 1July 2019Pages F218-F219 Copyright & PermissionsCopyright © 2019 the American Physiological Societyhttps://doi.org/10.1152/ajprenal.zh2-8726-corr.2019PubMed31282741History Published online 8 July 2019 Published in print 1 July 2019 Metrics