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A role for angiotensin II AT₁ receptors in ureteric bud cell branching

Section of Pediatric Nephrology, Department of Pediatrics, Tulane University Health Sciences Center, New Orleans, Louisiana 70112

Submitted 12 November 2002 ; accepted in final form 18 March 2003

Gene-targeting studies in mice demonstrate that the renin-angiotensin system is required for the proper development of the renal medulla. In the absence of angiotensin II (ANG II) or the ANG II type 1 (AT₁) receptor, mice exhibit poor papillary development and a severe urinary-concentrating defect. These findings imply that the ureteric bud (UB) and its branches are targets for ANG II actions during renal development. However, direct evidence linking ANG II with UB-branching morphogenesis does not exist. Using immunohistochemistry, we demonstrated that UB-derived epithelia express angiotensinogen (Ao) and the AT₁ receptor during murine metanephrogenesis. Ao and AT₁ receptors are expressed in the UB branches and to a lesser extent in the stromal mesenchyme. AT₁ receptor expression in UB-derived epithelia increased from embryo day 12 to day 16 and was observed on both luminal and basolateral membranes. In accord with these findings, cultured murine UB cells express AT₁ receptor protein and mRNA. Treatment of UB cells cultured in three-dimensional type I collagen gels with ANG II (10^–7 to 10^–5 M) elicits a dose-related increase in the number of cells that have primary and secondary branches. These effects of ANG II on UB branching are abrogated by pretreatment with the AT₁ receptor antagonist candesartan. These data demonstrate a direct and independent role for ANG II acting via AT₁ receptors on UB cell branching in vitro. The presence of Ao in the stroma and AT₁ on UB cells supports the notion that cross talk between stroma and epithelial cells is crucial to epithelial branching morphogenesis in the developing kidney.

kidney development; renin

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