[The expression of AT1A receptor and its modulation by benazepril in the renal tubulointerstitial lesions induced by ureteral obstruction].

OBJECTIVE

To study the expressions of angiotensin II 1A receptor (AT1A) both at the mRNA level and the protein level and their modulation by an angiotensin converting enzyme inhibitor, benazepril, in the renal tubulointerstitial injuries induced by unilateral ureteral obstruction (UUO) in rats.

METHODS

Six SD rats (UUO-T) were administered benazepril in the drinking water (50mg/L). Additional 6 rats were used as untreated controls (UUO-C). Mean arterial Prossure (MAP) was measured at the 10th day after UUO, and then all animals were sacrificed. The expressions of AT1A were examined both at the mRNA level by in situ hybridization using a subtype-specific probe and at the protein level by an immunohistochemistry methods using AT1 receptor antibody in normal rat kidneys and the obstructed rat kidneys.

RESULTS

MAP was 14.2 +/- 0. 6kPa in the UUO-T and 16.6 +/- 0.7kPa in the UUO-C (P < 0.05). Benazepril slowed the tubulointerstitial fibrosis (TIF) and reduced the expression of AT1A in the renal tubular epithelial cells, the interstitial areas, and the walls of renal arteriole in the UUO-T group.

CONCLUSION

The increased expressions of AT1A were found in the acute renal tubulointerstitial pathogenesis induced by UUO. Benazepril may retard the progression of TIF and decrease the expression of AT1A in the obstructed kidneys. We conclude that the effects of Ang II on the obstructed kidneys may be due to its binding with AT1A.