Igf-i receptor binding, autophosphorylation and kinase activity in
kidney and muscle of acutely uremic rats.
Tsao, Tanny, Fay W. Hsu, and Ralph Rabkin.
Research Service, Veterans Affairs Palo Alto Health Care System and
Stanford University, Palo Alto, California 94304, USA
APStracts 3:0211F, 1996.
Following acute tubular necrosis (ATN) kidney plasma membrane IGF-I
receptor number increases markedly though IGF-I mRNA levels do not
change. To determine whether this increase could represent a
redistribution of intracellular receptors and whether receptor
function is intact in acute uremia, rats with ATN of two days
duration and pair fed controls were studied. While skeletal muscle
receptor binding was unchanged, binding to receptors in solubilized
cortex and isolated cortical plasma membranes increased significantly
due to an increase in receptor number. However the increase in
membrane binding was 3 fold greater than the increase in solubilized
cortex binding. This indicates that the increase in total cellular
IGF-I receptors can only account for a minor portion of the increase
in abundance of plasma membrane receptors number and is consistent
with a redistribution of receptors from an intracellular to a
membrane location as the major mechanism. Autophosphorylation and
receptor kinase activity were unaffected by the uremia (BUN 198
mg/dl). Since these early steps of IGF-I receptor signalling are
intact early in acute uremia, it is likely that at this time in the
course of the disease the increase in receptor number will heighten
the sensitivity to IGF-I and may thus favor its participation in
renal repair.
Received 3 July 1996; accepted in final form 13 November 1996.
APS Manuscript Number F185-6.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996