{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T05:11:21Z","timestamp":1787893881670,"version":"build-2784847793"},"reference-count":41,"publisher":"SAGE Publications","issue":"3","license":[{"start":{"date-parts":[[2016,7,1]],"date-time":"2016-07-01T00:00:00Z","timestamp":1467331200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Renin Angiotensin Aldosterone Syst"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:sec>\n                    <jats:title>Objective:<\/jats:title>\n                    <jats:p>The Dahl salt-sensitive rat is a well-established model of salt-sensitive hypertension. The goal of this study was to assess the expression and activity of renal sodium channels and transporters in the renin-deficient salt-sensitive rat.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods:<\/jats:title>\n                    <jats:p>\n                      Renin knockout (Ren\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ) rats created on the salt-sensitive rat background were used to investigate the role of renin in the regulation of ion transport in salt-sensitive hypertension. Western blotting and patch-clamp analyses were utilized to assess the expression level and activity of Na\n                      <jats:sup>+<\/jats:sup>\n                      transporters.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results:<\/jats:title>\n                    <jats:p>\n                      It has been described previously that Ren\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      rats exhibit severe kidney underdevelopment, polyuria, and lower body weight and blood pressure compared to their wild-type littermates. Here we found that renin deficiency led to decreased expression of sodium-hydrogen antiporter (NHE3), the Na\n                      <jats:sup>+<\/jats:sup>\n                      \/H\n                      <jats:sup>+<\/jats:sup>\n                      exchanger involved in Na\n                      <jats:sup>+<\/jats:sup>\n                      absorption in the proximal tubules, but did not affect the expression of Na-K-Cl cotransporter (NKCC2), the main transporter in the loop of Henle. In the distal nephron, the expression of sodium chloride cotransporter (NCC) was lower in Ren\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      rats. Single-channel patch clamp analysis detected decreased ENaC activity in Ren\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      rats which was mediated via changes in the channel open probability.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion:<\/jats:title>\n                    <jats:p>These data illustrate that renin deficiency leads to significant dysregulation of ion transporters.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1470320316653858","type":"journal-article","created":{"date-parts":[[2016,7,21]],"date-time":"2016-07-21T21:12:41Z","timestamp":1469135561000},"update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":19,"title":["Renal sodium transport in renin-deficient Dahl salt-sensitive rats"],"prefix":"10.1177","volume":"17","author":[{"given":"Tengis S","family":"Pavlov","sequence":"first","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vladislav","family":"Levchenko","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daria V","family":"Ilatovskaya","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carol","family":"Moreno","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of Wisconsin, USA"},{"name":"Cardiovascular and Metabolic Diseases, MedImmune, Cambridge, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander","family":"Staruschenko","sequence":"additional","affiliation":[{"name":"Department of Physiology, Medical College of 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