Mechanism of adenosine-mediated decreases in glomerular filtration rate in dogs.

Abstract

This study evaluates the contributions of pre-and postglomerular resistances and glomerular capillary ultrafiltration coefficient (K f ) in adenosine-induced decreases in glomerular filtration rate (GFR).Experiments were performed on 19 dogs prepared for micropuncture.Whole kidney and superficial nephron functions were measured before and during adenosine infusion (0.1 /umol/min) into the renal artery.Whole kidney GFR decreased from 29.0 ± 1.7 to 23.1 ± 1.6 (SE) ml/min (P< 0.003).Renal plasma flow (RPF) increased slightly from 98 ± 6 to 108 ± 8 ml/min (P< 0.05), resulting in a decreased filtration fraction from 0.30 ± 0.02 to 0.22 ± 0.02.Superficial single nephron GFR and plasma flow decreased from 68.8 ± 5.2 to 39.9 ± 6.4 nl/min (P < 0.001) and from 206 ± 28 to 128 ± 17 nl/min (P < 0.01), respectively.Free flow and stop flow pressures in proximal tubules decreased from 23 ± 1 to 16 ± 1 mm Hg and from 44 ± 1 to 31 ± 2 mm Hg, respectively.K f was not significantly changed (2.55 ± 0.22 vs. 3.12 ± 0.88 nl/min per mm Hg).The hydrostatic pressures in efferent arterioles decreased from 14 ± 0.6 to 10.4 ± 1.8 mm Hg (P < 0.01).The resistance in the afferent arterioles increased more than 2-fold from 1.38 ± 0.25 to 3.04 ± 0.42 • 10 10 dynes • sec • cm" 5 (P < 0.003), whereas efferent arteriolar resistance was only slightly increased from 1.35 ± 0.18 to 1.76 ± 0.17.We conclude that intrarenal infusion of adenosine preferentially constricts the afferent arterioles of the superficial cortex and thereby decreases superficial GFR without decreases in glomerular capillary ultrafiltration coefficient.