title: Glucocorticoid restores the deterioration of water transport in the peritoneum through increment in aquaporin.
abstract: This study was carried out to investigate the role of aquaporin (AQP) in the peritoneum undergoing continuous ambulatory peritoneal dialysis (CAPD). Furthermore, we examined the effects of treatment with prednisolone (PSL) in a rat model of peritoneal sclerosis. We modelled peritoneal sclerosis by using dialysis solution with the addition of 0.1% chlorhexidine gluconate (CHG) for 10 days. Twenty male Wistar Kyoto (WKY) rats were divided into four groups and dialyzed with various solutions: (1) saline (NS group, n = 5); (2) 10% glucose (TZ group, n = 5); (3) 0.1% CHG (CHG group, n = 5); and (4) 0.1% CHG plus PSL (CHG + PSL group, n = 5). Expression of mRNA of AQPs (AQP-1-AQP-4) was studied by semi-quantitative reverse-transcription polymerase chain reaction (RT-PCR). Expression of AQP-4 was also measured by Western blot analysis. Ultrafiltration volume and peritoneal function were measured by the peritoneal equilibration test. In the TZ group, expression of AQP-1 and AQP-4 were significantly enhanced, in parallel with an increment in ultrafiltration volume. On the other hand, in the CHG group, expression of AQP-1 and AQP-4 were significantly suppressed, and ultrafiltration volume was lost. The use of PSL with CHG completely restored the expression of AQP-1 and AQP-4, and peritoneal function improved. No expression of AQP-2 and AQP-3 was seen in the peritoneum. Our results suggest that AQP-1 and AQP-4 may be important factors in water transport in patients undergoing CAPD. PSL might be an effective treatment to prevent the progress of peritoneal sclerosis in patients undergoing CAPD.
authors.affiliation: Department of Nephrology, Saitama Medical School, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Imai
authors.forename: H
authors.initials: H
authors.lastname: Nakamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Ishida
authors.forename: T
authors.initials: T
authors.lastname: Inoue
authors.forename: Y
authors.initials: Y
authors.lastname: Kanno
authors.forename: H
authors.initials: H
authors.lastname: Okada
authors.forename: S
authors.initials: S
authors.lastname: Suzuki
authors.forename: H
authors.initials: H
authors.lastname: Okano
authors.forename: H
authors.initials: H
authors.lastname: Suzuki
mesh_terms: D000818:Animals; D020346:Aquaporins / Q000378:metabolism*; D001692:Biological Transport / Q000187:drug effects; D015153:Blotting, Western; D001834:Body Water / Q000378:metabolism*; D002710:Chlorhexidine / Q000031:analogs & derivatives* / Q000494:pharmacology; D015314:Dialysis Solutions / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology*; D005947:Glucose / Q000494:pharmacology; D008297:Male; D010531:Peritoneal Dialysis, Continuous Ambulatory; D010537:Peritoneum / Q000378:metabolism* / Q000473:pathology; D011239:Prednisolone / Q000494:pharmacology*; D051381:Rats; D011921:Rats, Inbred WKY; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012598:Sclerosis; D012965:Sodium Chloride / Q000494:pharmacology
chemical_list: D020346:Aquaporins; D015314:Dialysis Solutions; D005938:Glucocorticoids; D012965:Sodium Chloride; D011239:Prednisolone; D005947:Glucose; C010882:chlorhexidine gluconate; D002710:Chlorhexidine