Mechanism of adenosine-mediated decreases in glomerular filtration rate in dogs.
Author(s) -
Hartmut Oßwald,
W. S. Spielman,
Franklyn G. Knox
Publication year - 1978
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/01.res.43.3.465
Subject(s) - mechanism (biology) , adenosine , renal function , chemistry , filtration (mathematics) , medicine , endocrinology , cardiology , mathematics , philosophy , epistemology , statistics
This study evaluates the contributions of pre- and postglomerular resistances and glomerular capillary ultrafiltration coefficient (Kf) 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 μmol/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. Kf 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 − 1010 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.
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