Your browser doesn't support javascript.
loading
Urinary excretion of AQP2 and ENaC in autosomal dominant polycystic kidney disease during basal conditions and after a hypertonic saline infusion.
Graffe, Carolina Cannillo; Bech, Jesper Nørgaard; Lauridsen, Thomas Guldager; Pedersen, Erling Bjerregaard.
Afiliación
  • Graffe CC; Dept. of Medical Research, Holstebro Hospital, Lægaardvej 12, Holstebro, Denmark. ccannillo@hotmail.com
Am J Physiol Renal Physiol ; 302(8): F917-27, 2012 Apr 15.
Article en En | MEDLINE | ID: mdl-22262484
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 ß-subunit of ENaC (u-ENaC(ß)), 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(ß), 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(ß), 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(ß) 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(ß).
Asunto(s)

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Solución Salina Hipertónica / Riñón Poliquístico Autosómico Dominante / Acuaporina 2 / Canales Epiteliales de Sodio Tipo de estudio: Clinical_trials Límite: Adolescent / Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Am J Physiol Renal Physiol Asunto de la revista: FISIOLOGIA / NEFROLOGIA Año: 2012 Tipo del documento: Article País de afiliación: Dinamarca Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Solución Salina Hipertónica / Riñón Poliquístico Autosómico Dominante / Acuaporina 2 / Canales Epiteliales de Sodio Tipo de estudio: Clinical_trials Límite: Adolescent / Adult / Aged / Female / Humans / Male / Middle aged Idioma: En Revista: Am J Physiol Renal Physiol Asunto de la revista: FISIOLOGIA / NEFROLOGIA Año: 2012 Tipo del documento: Article País de afiliación: Dinamarca Pais de publicación: Estados Unidos