Prostaglandins do not mediate impaired autoregulation or increased renin secretion in remnant rat kidneys

The rat remnant kidney model, produced by approximately five-sixths reduction in functional renal mass, is characterized by renal vasodilation, impaired autoregulation, and increased activity of the renin-angiotensin system. The present studies were designed to investigate the role of vasodilatory prostaglandins (PGs) in the altered hemodynamics in the remnant kidney. Four weeks post-ablation, renal blood flow (RBF), was significantly higher in rats fed a standard protein (SP) diet (n = 16) compared with low-protein-fed (LP) rats (n = 7) (6.2 +/- 0.6 vs. 3.7 +/- 0.5 ml/min; P < 0.01), autoregulation was impaired in SP rats [autoregulation index (AI) 1.0 +/- 0.1 (SP) vs. 0.2 +/- 0.1 (LP); P < 0.05], and renin secretory rates were significantly increased in SP rats both during the basal state [24 +/- 7 (SP) vs. 2 +/- 1 (LP) ng.ml-1 x h-1 x min-1; P < 0.05] and after reduction in renal perfusion pressure [110 +/- 29 (SP) vs. 16 +/- 7 (LP); P < 0.05]. Indomethacin administration (5 mg/kg bolus + 5 mg.kg-1 x h-1 infusion) in additional SP rats (n = 11) decreased RBF from 7.4 +/- 1.1 to 5.9 +/- 1.0 ml/min (P < 0.05) without improvement in autoregulation (AI = 1.1 +/- 0.3). Renin basal secretory rate and response to decreased renal perfusion pressure were not altered by indomethacin. These data suggest that PGs contribute to the renal vasodilation in the rat remnant kidney model, but they do not mediate the impaired renal autoregulation or the increased renin release.