{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T16:36:57Z","timestamp":1788194217628,"version":"build-2803163510"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2003,5]]},"abstract":"<jats:p>\n            We carried out semiquantitative immunoblotting of kidney to identify apical sodium transporter proteins whose abundances are regulated by angiotensin II. In NaCl-restricted rats (0.5 mEq Na\/200 g BW\/d), the type 1 angiotensin II receptor (AT\n            <jats:sub>1<\/jats:sub>\n            receptor) antagonist, candesartan, (1 mg\/kg of body weight per day SC for 2 days) markedly decreased the abundance of the \u03b1 subunit of the epithelial sodium channel (ENaC). This subunit has been shown to be rate-limiting for assembly of mature ENaC complexes. In addition, systemic infusion of angiotensin II increased \u03b1ENaC protein abundance in rat kidney cortex. The decrease in \u03b1ENaC protein abundance in response to AT\n            <jats:sub>1<\/jats:sub>\n            receptor blockade was associated with a fall in \u03b1ENaC mRNA abundance (real-time RT-PCR), consistent with transcriptionally mediated regulation. The effect of AT\n            <jats:sub>1<\/jats:sub>\n            receptor blockade on \u03b1ENaC expression was not blocked by spironolactone, suggesting a direct role of the AT\n            <jats:sub>1<\/jats:sub>\n            receptor in regulation of \u03b1ENaC gene expression. Candesartan administration was also found to increase the abundances of the \u03b2 and \u03b3 subunits. The increase in \u03b2 and \u03b3ENaC protein abundance was not associated with a significant increase in the renal abundances of the corresponding mRNAs, suggesting a posttranscriptional mechanism. Immunocytochemistry confirmed the increase in \u03b2 and \u03b3ENaC protein abundance and demonstrated candesartan-induced ENaC internalization in collecting duct cells. The results support the view that the angiotensin II receptor regulates ENaC abundance, consistent with a role for angiotensin II in regulation of collecting duct function.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000066129.12106.e2","type":"journal-article","created":{"date-parts":[[2003,5,1]],"date-time":"2003-05-01T20:28:48Z","timestamp":1051820928000},"page":"1143-1150","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":142,"title":["Long-Term Regulation of ENaC Expression in Kidney by Angiotensin II"],"prefix":"10.1161","volume":"41","author":[{"given":"Kathleen T.","family":"Beutler","sequence":"first","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shyama","family":"Masilamani","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sharon","family":"Turban","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jakob","family":"Nielsen","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Heddwen L.","family":"Brooks","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shana","family":"Ageloff","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Robert A.","family":"Fenton","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Randall K.","family":"Packer","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[{"name":"From the Laboratory of Kidney and Electrolyte Metabolism, NHLBI, National Institutes of Health (K.T.B., S.M., S.T., J.N., H.L.B., S.A., R.A.F., M.A.K.), Bethesda, Md; and Department of Biological Sciences, George Washington University (K.T.B., R.K.P.), Washington, DC."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_1_1_2","first-page":"S258","volume":"10","year":"1999","unstructured":"Hall JE, Brands MW, Henegar JR. 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