{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T11:40:26Z","timestamp":1791286826163,"version":"4.1.0"},"reference-count":62,"publisher":"American Physiological Society","issue":"5","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2003,11]]},"abstract":"<jats:p>Urinary tract obstruction impairs urinary concentrating capacity and reabsorption of sodium. To clarify the molecular mechanisms of these defects, expression levels of renal sodium transporters were examined in rats with 24-h bilateral ureteral obstruction (BUO) or at day 3 or 14 after release of BUO (BUO-R). BUO resulted in downregulation of type 3 Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger (NHE3) to 41 \u00b1 14%, type 2 Na-Pi cotransporter (NaPi-2) to 26 \u00b1 6%, Na-K-ATPase to 67 \u00b1 8%, type 1 bumetanide-sensitive Na-K-2Cl cotransporter (BSC-1) to 20 \u00b1 7%, and thiazide-sensitive cotransporter (TSC) to 37 \u00b1 9%. Immunocytochemistry confirmed downregulation of NHE3, NaPi-2, Na-K-ATPase, BSC-1, and TSC. Consistent with this downregulation, BUO-R was associated with polyuria, reduced urinary osmolality, and increased urinary sodium and phosphate excretion. BUO-R for 3 days caused a persistant downregulation of NHE3 to 53 \u00b1 10%, NaPi-2 to 57 \u00b1 9%, Na-K-ATPase to 62 \u00b1 8%, BSC-1 to 50 \u00b1 12%, and TSC to 56 \u00b1 16%, which was associated with a marked reduction in the net renal reabsorption of sodium (616 \u00b1 54 vs. 944 \u00b1 24 \u03bcmol \u00b7 min<jats:sup>-1<\/jats:sup>\u00b7 kg<jats:sup>-1<\/jats:sup>; P &lt; 0.05) and phosphate (6.3 \u00b1 0.9 vs. 13.1 \u00b1 0.4 \u03bcmol \u00b7 min<jats:sup>-1<\/jats:sup>\u00b7 kg<jats:sup>-1<\/jats:sup>; P &lt; 0.05) demonstrating a defect in renal sodium and phosphate reabsorption capacity. Moreover, downregulation of Na-K-ATPase and TSC persisted in BUO-R for 14 days, whereas NHE3, NaPi-2, and BSC-1 were normalized to control levels. In conclusion, downregulation of renal Na transporters in rats with BUO and release of BUO are likely to contribute to the associated urinary concentrating defect, increased urinary sodium excretion, and postobstructive polyuria.<\/jats:p>","DOI":"10.1152\/ajprenal.00170.2003","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:39:33Z","timestamp":1425415173000},"page":"F889-F901","source":"Crossref","is-referenced-by-count":59,"title":["Altered expression of major renal Na transporters in rats with bilateral ureteral obstruction and release of obstruction"],"prefix":"10.1152","volume":"285","author":[{"given":"Chunling","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Weidong","family":"Wang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tae-Hwan","family":"Kwon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark A.","family":"Knepper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f8rgen","family":"Fr\u00f8ki\u00e6r","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1995.404"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.243"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1985.173"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1979.237.1.F14"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1996.139"},{"key":"REF6","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1993.265.5.F736"},{"key":"REF7","doi-asserted-by":"publisher","DOI":"10.1172\/JCI108728"},{"key":"REF8","doi-asserted-by":"publisher","DOI":"10.1172\/JCI111677"},{"key":"REF9","doi-asserted-by":"publisher","DOI":"10.1111\/j.1464-410X.1991.tb15277.x"},{"key":"REF10","doi-asserted-by":"publisher","DOI":"10.1038\/ki.1980.57"},{"key":"REF11","doi-asserted-by":"crossref","unstructured":"Ecelbarger CA, Knepper MA, and Verbalis JG.Increased abundance of distal sodium transporters in rat kidney during vasopressin escape.J Am Soc Nephrol12: 207-217, 2001.","DOI":"10.1681\/ASN.V122207"},{"key":"REF12","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.271.3.F619"},{"key":"REF13","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.1998.00984.x"},{"key":"REF14","doi-asserted-by":"publisher","DOI":"10.1046\/j.1523-1755.2000.00156.x"},{"key":"REF15","doi-asserted-by":"publisher","DOI":"10.1007\/BF00373984"},{"key":"REF16","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1981.241.3.F289"},{"key":"REF17","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1997.273.2.F213"},{"key":"REF18","doi-asserted-by":"publisher","DOI":"10.1152\/ajprenal.1996.270.4.F657"},{"key":"REF19","unstructured":"Curhan GCand Zeidel ML.Urinary tract obstruction. 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