Mechanisms of impaired urinary concentrating ability in adult rats treated neonatally with enalapril

摘要: Neonatal angiotensin-converting enzyme inhibition or angiotensin II type-1 receptor blockade induces irreversible renal histological abnormalities and an impaired urinary concentrating ability in the rat. The aim of present study was to determine pathophysiological mechanisms underlying defect urine concentration adult rats treated neonatally with enalapril. Male Wistar received daily intraperitoneal injections enalapril (10 mg kg(-1)) saline vehicle from 3 24 days age. Assessments fluid handling maximal osmolality (Uosm(max)), function tubular free water reabsorption (T(c)H2O) under pentobarbital anaesthesia, tissue solute concentrations, aquaporin-2 (AQP2) expression, kidney histology, were performed 12-16-week-old rats. Uosm(max) (1488 +/- 109 vs. 2858 116 mosm kg(-1), P < 0.05) T(c)H2O reduced enalapril- vehicle-treated after administration 1-desamino-8-D-arginine vasopressin. Neonatally enalapril-treated showed marked papillary atrophy, a decrease medullary reduction AQP2 expression specifically inner medulla. Glomerular filtration rate, plasma flow excretion rates sodium, potassium chloride did not differ between groups. In conclusion, origin which primarily could be explained by atrophy. However, generate interstitial hypertonicity, also seem contribute this defect.