DELETERIOUS EFFECTS OF CALCIUM-CHANNEL BLOCKADE ON PRESSURE TRANSMISSION AND GLOMERULAR INJURY IN RAT REMNANT KIDNEYS

Hypertensive mechanisms are postulated to play a major role in the pro gressive glomerulosclerosis (GS) after renal mass reduction, But, in c ontrast to converting enzyme inhibitors, BP reduction by calcium chann el blockers, has not provided consistent protection, Radiotelemetric B P monitoring for 7 wk was used to compare nifedipine (N) and enalapril (E) in the rat similar to 5/6 renal ablation model, After the first w eek, rats received N, E, or no treatment (C), The overall averaged sys tolic BP in C (173+/-7 mmHg) was reduced by both E and N (P < 0.001), but E was more effective (113+/-2 vs. 134+/-3 mmHg, P < 0.01), GS was prevented by E (2+/-1 vs, 26+/-5% in C) but not by N (25+/-6%), GS cor related well with the overall averaged BP in individual animals of all groups, but the slope of the relationship was significantly steeper i n N compared with C + E rats (P < 0.02), suggesting greater pressure t ransmission to the glomeruli and GS for any given BP, Since autoregula tory mechanisms provide the primary protection against pressure transm ission, renal autoregulation was examined at 3 wk in additional rats, Autoregulation was impaired in C rats, was not additionally altered by E, but was completely abolished by N, These data demonstrate the impo rtance of autoregulatory mechanisms in the pathogenesis of hypertensiv e injury and suggest that calcium channel blockers which adversely aff ect pressure transmission may not provide protection despite significa nt BP reduction.