{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T13:28:15Z","timestamp":1773754095092,"version":"3.50.1"},"reference-count":47,"publisher":"American Physiological Society","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2012,4,15]]},"abstract":"<jats:p>Renal handling of sodium and water is abnormal in chronic kidney diseases. To study the function and regulation of the aquaporin-2 water channel (AQP2) and the epithelial sodium channel (ENaC) in autosomal dominant polycystic kidney disease (ADPKD), we measured urinary excretion of AQP2 (u-AQP2), the \u03b2-subunit of ENaC (u-ENaC<jats:sub>\u03b2<\/jats:sub>), cAMP (u-cAMP), and prostaglandin E<jats:sub>2<\/jats:sub>(u-PGE<jats:sub>2<\/jats:sub>); free water clearance (C<jats:sub>H2O<\/jats:sub>); fractional sodium excretion (FE<jats:sub>Na<\/jats:sub>); and plasma vasopressin (p-AVP), renin (p-Renin), angiotensin II (p-ANG II), aldosterone (p-Aldo), and atrial and brain natriuretic peptide (p-ANP, p-BNP) in patients with ADPKD and healthy controls during 24-h urine collection and after hypertonic saline infusion during high sodium intake (HS; 300 mmol sodium\/day) and low sodium intake (LS; 30 mmol sodium\/day). No difference in u-AQP2, u-ENaC<jats:sub>\u03b2<\/jats:sub>, u-cAMP, u-PGE<jats:sub>2<\/jats:sub>, C<jats:sub>H2O<\/jats:sub>, and vasoactive hormones was found between patients and controls at baseline, but during HS the patients had higher FE<jats:sub>Na<\/jats:sub>. The saline caused higher increases in FE<jats:sub>Na<\/jats:sub>in patients than controls during LS, but the changes in u-ENaC<jats:sub>\u03b2<\/jats:sub>, p-Aldo, p-ANP, p-BNP, p-Renin, and p-ANG II were similar. Higher increases in u-AQP2 and p-AVP were seen in patients during both diets. In conclusion, u-AQP2 and u-ENaC<jats:sub>\u03b2<\/jats:sub>were comparable in patients with ADPKD and controls at baseline. In ADPKD, the larger increase in u-AQP2 and p-AVP in response to saline could reflect an abnormal water absorption in the distal nephron. During LS, the larger increase in FE<jats:sub>Na<\/jats:sub>in response to saline could reflect a defective renal sodium retaining capacity in ADPKD, unrelated to changes in u-ENaC<jats:sub>\u03b2<\/jats:sub>.<\/jats:p>","DOI":"10.1152\/ajprenal.00616.2011","type":"journal-article","created":{"date-parts":[[2012,1,19]],"date-time":"2012-01-19T05:52:35Z","timestamp":1326952355000},"page":"F917-F927","source":"Crossref","is-referenced-by-count":15,"title":["Urinary excretion of AQP2 and ENaC in autosomal dominant polycystic kidney disease during basal conditions and after a hypertonic saline infusion"],"prefix":"10.1152","volume":"302","author":[{"given":"Carolina Cannillo","family":"Graffe","sequence":"first","affiliation":[{"name":"Departments of 1Medical Research and"},{"name":"University of Aarhus, Aarhus, Denmark"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jesper N\u00f8rgaard","family":"Bech","sequence":"additional","affiliation":[{"name":"Departments of 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