{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T07:16:16Z","timestamp":1788160576092,"version":"build-2803163510"},"reference-count":59,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T00:00:00Z","timestamp":1788134400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100002850","name":"Fondo Nacional de Desarrollo Cient\u00edfico y Tecnol\u00f3gico","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100002850","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Pharmacol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Activation of the intrarenal renin\u2013angiotensin system (RAS) is a key mechanism driving sodium retention and hypertension. In the distal nephron, locally generated angiotensin II (Ang II) promotes Na\n                      <jats:sup>+<\/jats:sup>\n                      reabsorption through coordinated regulation of the epithelial Na\n                      <jats:sup>+<\/jats:sup>\n                      channel (ENaC) in principal cells and electroneutral NaCl transport mediated by pendrin and the Na\n                      <jats:sup>+<\/jats:sup>\n                      -dependent Cl\n                      <jats:sup>\u2212<\/jats:sup>\n                      \/HCO3\n                      <jats:sup>\u2212<\/jats:sup>\n                      exchanger (NDCBE) in intercalated cells. Emerging evidence identifies \u03b1-ketoglutarate as an intrarenal paracrine signal acting through oxoglutarate receptor 1 (OXGR1), which is highly expressed in collecting duct intercalated cells. We hypothesized that OXGR1 is required to couple intrarenal RAS activation with collecting duct Na\n                      <jats:sup>+<\/jats:sup>\n                      transport and blood pressure regulation during Ang II-dependent hypertension.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      mice were subjected to chronic Ang II infusion (400 ng\u00b7min\n                      <jats:sup>-1<\/jats:sup>\n                      \u00b7kg\n                      <jats:sup>-1<\/jats:sup>\n                      , 14 days) using two approaches: pharmacological OXGR1 blockade with montelukast (3.5 \u03bcg \u00b7min\n                      <jats:sup>-1<\/jats:sup>\n                      \u00b7kg\n                      <jats:sup>-1<\/jats:sup>\n                      ) and global OXGR1 genetic deletion (OXGR1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      ). Blood pressure, Na\n                      <jats:sup>+<\/jats:sup>\n                      balance, and the renal abundance of pendrin, NDCBE and \u03b1ENaC were assessed. Intrarenal RAS activity was evaluated by measuring Ang I (renin activity), Ang II, ACE activity and (pro)renin receptor (PRR).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Ang II infusion increased blood pressure, promoted antinatriuresis, and elevated intrarenal Ang II, ACE activity, PRR, pendrin, and \u03b1ENaC protein abundance. In contrast, both montelukast-treated wild type and OXGR1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice infused with Ang II displayed attenuated hypertensive responses, reduced Na\n                      <jats:sup>+<\/jats:sup>\n                      retention, and failed to increase intrarenal Ang II, pendrin, or \u03b1ENaC abundance.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      These findings identify OXGR1 as a critical regulator linking intrarenal RAS activation to distal nephron Na\n                      <jats:sup>+<\/jats:sup>\n                      transport and suggest that OXGR1-dependent signaling contributes to sodium retention and the development of Ang II-induced hypertension.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fphar.2026.1869136","type":"journal-article","created":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T06:49:00Z","timestamp":1788158940000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["Loss of OXGR1 function uncouples intrarenal RAS activation from pendrin and \u03b1ENaC regulation and blunts angiotensin II-induced hypertension"],"prefix":"10.3389","volume":"17","author":[{"given":"Pilar","family":"C\u00e1rdenas","sequence":"first","affiliation":[{"name":"Laboratory of Biological Chemistry, Institute of Chemistry, Pontificia Universidad Cat\u00f3lica de Valpara\u00edso","place":["Valpara\u00edso, Chile"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Juan","family":"Castillo-Geraldo","sequence":"additional","affiliation":[{"name":"Laboratory of Biological Chemistry, Institute of Chemistry, Pontificia Universidad Cat\u00f3lica de 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Moura","family":"Bello","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Universidade Federal de S\u00e3o Paulo (UNIFESP\/EPM)","place":["Sao Paulo, Brazil"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriel","family":"Joo-Mulsow","sequence":"additional","affiliation":[{"name":"Facultad de Medicina, Instituto de Ciencias Biom\u00e9dicas, Universidad de Chile","place":["Santiago, Chile"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Luis","family":"Michea","sequence":"additional","affiliation":[{"name":"Facultad de Medicina, Instituto de Ciencias Biom\u00e9dicas, Universidad de Chile","place":["Santiago, Chile"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dulce Elena","family":"Casarini","sequence":"additional","affiliation":[{"name":"Nephrology Division, Department of Medicine, Universidade Federal de S\u00e3o Paulo (UNIFESP\/EPM)","place":["Sao Paulo, 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