ANGIOTENSIN TYPE II RECEPTOR EXPRESSION AND URETERAL BUDDING

No AccessJournal of UrologyPEDIATRIC UROLOGY1 Nov 2001ANGIOTENSIN TYPE II RECEPTOR EXPRESSION AND URETERAL BUDDING KEISUKE OSHIMA, YOICHI MIYAZAKI, JOHN W. BROCK, MARK C. ADAMS, IEKUNI ICHIKAWA, and JOHN C. POPE KEISUKE OSHIMAKEISUKE OSHIMA More articles by this author , YOICHI MIYAZAKIYOICHI MIYAZAKI More articles by this author , JOHN W. BROCKJOHN W. BROCK More articles by this author , MARK C. ADAMSMARK C. ADAMS More articles by this author , IEKUNI ICHIKAWAIEKUNI ICHIKAWA More articles by this author , and JOHN C. POPEJOHN C. POPE More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(05)65703-5AboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail Abstract Purpose: Deletion of the angiotensin type II receptor gene (Agtr2) in mice results in a spectrum of urinary tract anomalies similar to that in humans. The mechanism behind this anomalous development is poorly understood. We evaluated Agtr2 expression as it relates to normal and abnormal ureteral budding. Materials and Methods: A total of 400 wild type mice were inspected at birth for gross evidence of a urinary tract anomaly. In addition, the urinary tracts of 30 wild type embryos were evaluated at 11.0/11.5 and 13.5 weeks of gestation. These embryos were examined for ureteral budding site via section and whole mount in situ hybridization with c-ret probe and Agtr2 expression via in situ hybridization with Agtr2 riboprobe. There were 740 newborn mice homozygous for the null mutation of Agtr2 also evaluated along with 55 angiotensin type II knockout embryos at the aforementioned gestational ages. Results: All wild type newborn animals were grossly normal. Of the angiotensin type II knockout newborns 23 (3.1%) had gross abnormalities of the urinary tract at birth. The predominant finding was a duplicated collecting system associated with a hydronephrotic upper pole moiety. These duplicated collecting systems fulfilled the Meyer-Weigert law. Interestingly, 25 (59.5%) of the knockout embryos showed abnormal ureteral budding. However, in wild type embryos Agtr2 was expressed at this “ectopic” cranial site between the wolffian duct and metanephric mesenchyme. Conclusions: Although not the sole regulator, angiotensin type II receptor expression may have a role in the embryological development of the urinary tract by inhibiting aberrant ureteral budding. A defect in this inhibitory process appears to cause ectopic ureteral budding, and may subsequently lead to renal dysplasia and other congenital anomalies of the kidney and urinary tract. References 1 : Fetal ureteric reflux. Br J Urol1987; 59: 291. Google Scholar 2 : Antenatal diagnosis of congenital abnormalities in the urinary tract. Results from the Northern Region Fetal Abnormality Survey. Br J Urol1988; 62: 295. 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Google Scholar 16 : Inductive tissue interactions, cell signaling, and the control of kidney organogenesis. Cell1997; 90: 975. Google Scholar From the Departments of Pediatric Urology and Nephrology, Vanderbilt Children’s Hospital, Vanderbilt University Medical Center, Nashville, Tennessee© 2001 by American Urological Association, Inc.FiguresReferencesRelatedDetailsCited bySANTIS W, PETERS C, YALLA S and SULLIVAN M (2018) Ureteral Function is Modulated by a Local Renin-Angiotensin SystemJournal of Urology, VOL. 170, NO. 1, (259-263), Online publication date: 1-Jul-2003. Volume 166Issue 5November 2001Page: 1848-1852 Advertisement Copyright & Permissions© 2001 by American Urological Association, Inc.KeywordshydronephrosisangiotensinsureterMetricsAuthor Information KEISUKE OSHIMA More articles by this author YOICHI MIYAZAKI More articles by this author JOHN W. BROCK More articles by this author MARK C. ADAMS More articles by this author IEKUNI ICHIKAWA More articles by this author JOHN C. POPE More articles by this author Expand All Advertisement PDF downloadLoading ...