title: Urinary excretion of AQP2 and ENaC in autosomal dominant polycystic kidney disease during basal conditions and after a hypertonic saline infusion.
abstract: 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 β-subunit of ENaC (u-ENaC(β)), cAMP (u-cAMP), and prostaglandin E(2) (u-PGE(2)); free water clearance (C(H2O)); fractional sodium excretion (FE(Na)); 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(β), u-cAMP, u-PGE(2), C(H2O), and vasoactive hormones was found between patients and controls at baseline, but during HS the patients had higher FE(Na). The saline caused higher increases in FE(Na) in patients than controls during LS, but the changes in u-ENaC(β), 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(β) 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(Na) in response to saline could reflect a defective renal sodium retaining capacity in ADPKD, unrelated to changes in u-ENaC(β).
authors.affiliation: Dept. of Medical Research, Holstebro Hospital, Lægaardvej 12, Holstebro, Denmark. ccannillo@hotmail.com
authors.forename: Carolina Cannillo
authors.initials: CC
authors.lastname: Graffe
authors.forename: Jesper Nørgaard
authors.initials: JN
authors.lastname: Bech
authors.forename: Thomas Guldager
authors.initials: TG
authors.lastname: Lauridsen
authors.forename: Erling Bjerregaard
authors.initials: EB
authors.lastname: Pedersen
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000450:Aldosterone / Q000097:blood; D000804:Angiotensin II / Q000097:blood; D051399:Aquaporin 2 / Q000652:urine*; D009320:Atrial Natriuretic Factor / Q000097:blood; D002908:Chronic Disease; D018592:Cross-Over Studies; D000242:Cyclic AMP / Q000652:urine; D015232:Dinoprostone / Q000652:urine; D053503:Epithelial Sodium Channels / Q000652:urine*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D020097:Natriuretic Peptide, Brain / Q000097:blood; D016891:Polycystic Kidney, Autosomal Dominant / Q000652:urine*; D012083:Renin / Q000097:blood; D012462:Saline Solution, Hypertonic / Q000008:administration & dosage*; D012964:Sodium / Q000652:urine; D014667:Vasopressins / Q000097:blood; D055815:Young Adult
chemical_list: C496023:AQP2 protein, human; D051399:Aquaporin 2; D053503:Epithelial Sodium Channels; D012462:Saline Solution, Hypertonic; D014667:Vasopressins; D000804:Angiotensin II; D020097:Natriuretic Peptide, Brain; D000450:Aldosterone; D009320:Atrial Natriuretic Factor; D012964:Sodium; D000242:Cyclic AMP; D012083:Renin; D015232:Dinoprostone