During intrarenal infusion of angiotensin I (AI) conversion to angiotensin II (AII) within the kidney has been shown to occur early enough to decrease glomerular filtration rate (GFR). To evaluate further the mechanism by which AI decreases GFR, micropuncture studies were conducted in sodium replete dogs. Feedback-mediated alterations in glomerular function were minimized by reducing renal arterial pressure to 90 mm Hg. During infusion of AI (0.82 ± 0.01 μg min-1), renal blood flow (3.91 ± 0.25 ml min-1 g-1) and GFR (0.63 ± 0.04 ml min-1 g-1) decreased by 36.7 ± 6.1% and 18.9 ± 6.1, respectively. Similarly, single nephron GFR decreased from 66.4 ± 3.8 to 40.0 ± 3.2 nl min-1 and estimated glomerular plasma flow (280 ± 49 nl min-1) decreased by 55 ± 6%. Stop-flow pressure (40.5 ± 3.6 mm Hg) did not change significantly, while proximal tubular (21.8 ± 1.4 mm Hg) and peritubular capillary pressures (13.2 ± 1.8 mm Hg) decreased by 225 ± 2.8% and 49.4% ± 5.1%, respectively. Glomerular capillary and effective filtration pressures were not altered significantly. There were increases in both preglomerular (168%) and efferent (203%) arteriolar resistances, along with a decrease in the glomerular filtration coefficient [K(f)] from 4.6 ± 0.6 to 2.5 ± 0.5 nl mm Hg-1 min-1. These data indicate that augmented intrarenal conversion of circulating AI reduces GFR as a consequence of decreases in K(f) as well as in glomerular plasma flow, the latter being due to concomitant increases in preglomerular and efferent arteriolar resistances.
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