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FILTRATION FAILURE INDUCED BY p AMINOPHENOL IN RATS IS DUE TO RAISED INTRATUBULAR PRESSURE AND NOT CHANGES IN GLOMERULAR FUNCTION
Author(s) -
Henry Mark A.,
Harris Peter J.,
Naughton Robert J.,
Walker Lesley L.,
Skinner Sandford L.,
Tange John D.
Publication year - 1990
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1990.tb01362.x
Subject(s) - tubular fluid , renal function , reabsorption , nephron , tubuloglomerular feedback , renal blood flow , chemistry , filtration fraction , medicine , blood flow , endocrinology , interstitial fluid , kidney , proximal tubule
SUMMARY 1. The p ‐aminophenol ( p AP) model of tubular necrosis displays elevated tubular pressures equivalent to ‘stop‐flow’, with low glomerular filtration rate (GFR) but maintained blood flow and urine output. Renal function, micropuncture, and morphological studies were performed in anaesthetized rats to examine the causes of filtration failure. 2. At the height of p AP‐induced renal failure proximal tubular fluid reabsorption (Jv (a) was markedly reduced while proximal and distal free‐flow rates measured by tubular fluid collections during venting of the nephron were not significantly different from saline‐injected controls. Renal blood flow was maintained over the 4 h observation period despite extensive and selective proximal tubular necrosis. There was no temporal relationship between increased tubular pressure and cast formation. 3. Maintained blood and tubular fluid flow rates indicate that activation of tubuloglomerular feedback plays little or no part in p AP‐induced renal failure, which is apparently due to high fluid flow resistance in the region of the connecting tubule, late distal convolution or collecting ducts. Morphological appearances were consistent with compression of these segments.