Bilateral renal function responses to converting enzyme inhibitor (SQ 20,881) in two-kidney, one clip Goldblatt hypertensive rats.

The influence of the renln-angiotensin system on individual kidney function of two-kidney, one clip Goldblatt hypertensive (GH) rats was evaluated by determining renal functional responses during intravenous infusion of converting enzyme inhibitor (CEI) (SQ 20,881, 0 J rag/100 g-hr) for 3.5 bourn. Rats were made hypertensive by placing a 0.25 mm silver clip on the right renal artery 3-4 weeks prior to study. Normal rats and GH rats were prepared to allow urine collections from each kidney. Mean arterial pressure of GH rats fell significantly from preinfusion levels of 153 7 to 126 4 mm Hg during CEI infusion. Despite this decrease in arterial pressure, the nondipped kidneys with reduced renal renin activity (14 5 vs 293 40 ng Al/mg-hr in the clipped kidney) exhibited dramatic increases in gtomerular filtration rate (GFR) (from 1.45 0.06 to 2.56 0.35 ml/mln), urine flow (4.82 0.71 to 9.11 1.19 ^il/mln), sodium excretion (0.10 0.02 to 1.15 0.39 M Eq/mln), fractional sodium excretion (0.05% 0.02% to 0.43% 0.18%), and potassium excretion (0.94 0.08 to 2.50 0.55 /<Eq/mln). Significant arterial-pressure-associated decreases In GFR, urine flow, and salt excretion were observed in the clipped kidney. In normal rats, CEI infusion produced reductions in arterial pressure and increases in GFR, urine flow, and sodium excretion that were of smaller magnitude than those observed in the nondipped kidneys of GH rats. Plasma renin activity was significantly higher in GH rats than in normal rats (24.0 2.7 vs 12.8 3.4 ng AI/mMir). The augmented renal responses to CEI by the nondipped kidney suggest that elevated circulating angiotensin levels exert a substantial influence on hemodynamic and excretory function of these kidneys even though intrarenal renin activity is markedly reduced. This influence may lead to fluid and electrolyte retention and may partially explain the apparent failure of the nondipped kidney to prevent the development of hypertension. (Hypertension 3: 285-293, 1981)