A functional renin-angiotensin system (RAS) is required for normal kidney development. Neonatal inhibition of RAS results in long-term pathological renal phenotype and causes accumulation of hyaluronan (HA), a glucoseaminoglycan involved in morphogenesis and inflammation. To elucidate the mechanisms, intrarenal HA content was followed during neonatal completion of nephrogenesis with or without angiotensin converting enzyme inhibition (ACEI) together with mRNA expression of hyaluronan synthases (HAS) and hyaluronidases (Hyal). In 6–8 days old control rats cortical HA content was high and reduced by 93% on days 10- 21, thereby reaching adult low levels. Medullary HA content was high on days 6–8 and then reduced by 85% to 12-fold above cortical levels at day 21. In neonatally ACEI-treated rats the reduction in HA was abolished. Temporal expression of HAS2 corresponded with reduction in HA content in normal kidney. In ACEI-treated animals cortical HAS2 remained twice the expression of controls. Medullary Hyal1 increased in controls but decreased in ACEI- treated animals. Urine hyaluronidase activity decreased with time in control animals while in ACEI-treated animals it was initially 50% lower and did not change over time. At 13 weeks the ACEI-treated animals showed reduced ability (– 53%) to concentrate urine during thirst provocation. In conclusion, the high renal HA content is rapidly reduced due to reduced HAS2 and increased Hyal1 mRNA expressions. Normal angiotensin II function is crucial for inducing these changes. Due to the extreme water- attracting and pro-inflammatory properties of HA, accumulation in the neonatally ACEI-treated kidneys may partly explain the phenotype of the adult kidney i.e. reduced urinary concentration ability and tubulointerstitial inflammation.