EFFECTS OF ANGIOTENSIN-CONVERTING ENZYME-INHIBITION ON GLOMERULAR NUMBER, JUXTAGLOMERULAR CELL-ACTIVITY AND RENIN CONTENT IN EXPERIMENTAL UNILATERAL HYDRONEPHROSIS

Objective: To determine the effects of hydronephrosis on glomerular nu mber and juxtaglomerular cell synthetic activity and the protective in fluence of angiotensin converting enzyme inhibition. Design: A compari son of sham and contralateral kidneys with 8-week ipsilateral ureteral ligated hydronephrotic kidneys in BALB/c mice. Enalapril was administ ered from 5 weeks in additional sham and hydronephrotic kidney groups. Methods: Renin and prorenin immunohistochemistry was applied to secti ons of perfusion-fixed kidneys at the light and electron microscope le vel. Glomerular number was estimated by a physical disector-fractionat or stereological method. An enzyme kinetic renin assay was performed i n kidney tissue and plasma. Results: Glomerular number in hydronephrot ic kidneys decreased significantly compared with sham and contralatera l kidneys. Renin content in hydronephrotic kidneys did not change comp ared with sham or contralateral kidneys, but the renin content in the glomerulus was significantly greater in hydronephrotic than in contral ateral kidneys and similar to in sham kidneys. Contralateral kidneys e nlarged significantly and their total renin content decreased signific antly compared with hydronephrotic and sham kidneys. Plasma renin was unchanged. Fewer juxtaglomerular cells were labelled for renin and pro renin in contralateral than in hydronephrotic or sham kidneys. Granulo poiesis and exocytotic profiles were markedly greater in hydronephroti c than in contralateral or sham kidneys. Following enalapril, glomerul ar number was significantly higher in hydronephrotic kidneys and renin content increased proportionally more in contralateral than in hydron ephrotic or sham kidneys. Conclusion: Hydronephrosis for 8 weeks resul ts in atrophy of 50% of glomeruli and exerts an inhibitory influence o n contralateral juxtaglomerular cells while augmenting ipsilateral ren in production per remaining glomerulus with maintenance of plasma reni n. Enalapril preserves glomeruli and reverses the contralateral inhibi tory influence, suggesting an angiotensin-related mechanism.