Distal Tubule [Na+] and juxtaglomerular apparatus Renin activity in uranyl nitrate induced acute renal failure in the rat. An evaluation of the role of tubuloglomerular feedback.

It has been previously demonstrated that single neophron filtration rate, whole kidney glomerular filtration rate and total renal blood flow decreased by 30-35% 6 h after uranyl nitrate induced acute renal failure in the rat. In order to evaluate a role of the renin-angiotensin system in the initiating phase (0-6 h) of this model of acute renal failure determinations of plasma renin activity, superficial (S) and deep (D) juxtaglomerular apparatus (JGA) renin activity and distal nephron [Na+] were obtained. Plasma renin activity increased from the control value of 1.5 +/- 0.3 (S.E.M.) to 2.9 +/- 0.4 ng/ml/h (P less than 0.005) at 6 h. Mean renin activity in S- and D-JGA's of control rats was 6.99 +/- 0.41 and 2.67 +/- 0.21 ng/JGA/h, respectively. After uranyl nitrate, renin activity in S-JGA's increased to 13.62 +/- 0.80 ng/JGA/h (P less than 0.001) at 2 h and remained elevated, 12.56 +/- 0.90 and 12.75 +/- 0.87 ng/JGA/h at 4 and 6 h. D-JGA renin activity increased (P less than 0.05) to 7.04 +/- 0.53, 6.23 +/- 0.31 and 3.44 +/- 0.33 ng/JGA/h at 2, 4 and 6 h after uranyl nitrate. Distal tubule [Na+], 27 samples in 6 rats, increased from a mean control value of 53.7 +/- 1.2 mEq/l to 116.9 +/- 2.5 mEq/l, 24 samples in 6 rats (P less than 0.001). Prompt increases in JGA renin activity were observed in the initiating phase of acute renal failure, suggesting a role for the renin-angiotensin system in the pathophysiology of this nephrotoxic model. The association of increased JGA renin activity and increased distal [Na+] is consistent with a role for the tubuloglomerular feedback mechanism in the initiating phase of uranyl nitrate induced acute renal failure in the rat.