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Male 129S2\/Sv mice were fed either K\n                    <jats:sup>+<\/jats:sup>\n                    -deficient, control, high-K\n                    <jats:sup>+<\/jats:sup>\n                    basic, or high-KCl diets for 10 days. Mice maintained on a K\n                    <jats:sup>+<\/jats:sup>\n                    -deficient diet exhibited no change in blood pressure, whereas K\n                    <jats:sup>+<\/jats:sup>\n                    -loaded mice developed an ~10-mmHg blood pressure increase. Following challenge with NaCl, K\n                    <jats:sup>+<\/jats:sup>\n                    -deficient mice developed a salt-sensitive 8 mmHg increase in blood pressure, whereas blood pressure was unchanged in mice fed high-K\n                    <jats:sup>+<\/jats:sup>\n                    diets. Notably, 10 days of K\n                    <jats:sup>+<\/jats:sup>\n                    depletion induced diabetes insipidus and upregulation of phosphorylated NaCl cotransporter, proximal Na\n                    <jats:sup>+<\/jats:sup>\n                    transporters, and pendrin, likely contributing to the K\n                    <jats:sup>+<\/jats:sup>\n                    -deficient NaCl sensitivity. While the anionic content with high-K\n                    <jats:sup>+<\/jats:sup>\n                    diets had distinct effects on transporter expression along the nephron, both K\n                    <jats:sup>+<\/jats:sup>\n                    basic and KCl diets had a similar increase in blood pressure. The blood pressure elevation on high-K\n                    <jats:sup>+<\/jats:sup>\n                    diets correlated with increased Na\n                    <jats:sup>+<\/jats:sup>\n                    -K\n                    <jats:sup>+<\/jats:sup>\n                    -2Cl\n                    <jats:sup>\u2212<\/jats:sup>\n                    cotransporter and \u03b3-epithelial Na\n                    <jats:sup>+<\/jats:sup>\n                    channel expression and increased urinary response to furosemide and amiloride. We conclude that the dietary K\n                    <jats:sup>+<\/jats:sup>\n                    maneuvers used here did not recapitulate the inverse effects of K\n                    <jats:sup>+<\/jats:sup>\n                    on blood pressure observed in human epidemiological studies. This may be due to the extreme degree of K\n                    <jats:sup>+<\/jats:sup>\n                    stress, the low-Na\n                    <jats:sup>+<\/jats:sup>\n                    -to-K\n                    <jats:sup>+<\/jats:sup>\n                    ratio, the duration of treatment, and the development of other coinciding events, such as diabetes insipidus. These factors must be taken into consideration when studying the physiological effects of dietary K\n                    <jats:sup>+<\/jats:sup>\n                    loading and depletion.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00527.2019","type":"journal-article","created":{"date-parts":[[2020,4,13]],"date-time":"2020-04-13T05:31:48Z","timestamp":1586755908000},"page":"F1341-F1356","source":"Crossref","is-referenced-by-count":51,"title":["Effects of extreme potassium stress on blood pressure and renal tubular sodium transport"],"prefix":"10.1152","volume":"318","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2350-3052","authenticated-orcid":false,"given":"Cary R.","family":"Boyd-Shiwarski","sequence":"first","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claire 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Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lubika J.","family":"Nkashama","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie M.","family":"Mutchler","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shawn E.","family":"Griffiths","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophia A.","family":"Knoell","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte Division, Department of 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