A role for protein kinase c in bradykinin mediated activation of
renal pelvic sensory receptors.
Kopp, Ulla C., and Lori A. Smith.
Department of Internal Medicine, University of Iowa College of
Medicine and Department of Veterans Affairs Medical Center, Iowa
City, Iowa 52242
APStracts 2:0064R, 1995.
In anesthetized rats, activation of renal pelvic sensory receptors by
bradykinin results in an increase in afferent renal nerve activity
(ARNA) that is dependent on intact renal prostaglandin synthesis.
Since bradykinin is a known activator of the phosphoinositide system
we examined whether the increase in ARNA produced by bradykinin
involved activation of protein kinase C (PKC). Renal pelvic perfusion
with the phorbol ester 4[beta]-phorbol 12,13-dibutyrate (PDBu, 1 _M),
increased ARNA (31+/-3%, p<0.01) in rats fed a normal diet but not
in rats fed an essential fatty acid deficient (EFAD) diet. Renal
pelvic perfusion with the PKC inhibitors calphostin C (1 _M),
staurosporine (20 nM) and H-7 (40 _M) reduced the ARNA responses to
bradykinin (20 _M) by 69+/-10, 76+/-10 and 77+/-10%, respectively
(all p<0.01). Pretreatment with PDBu (1 _M), known to cause a
feedback inhibition of bradykinin mediated activation of the
phosphoinositide system, reduced the ARNA response to bradykinin by
73+/-6% (p<0.01). Pretreatment with PDD was without effect. These
findings suggest that activation of PKC contributes importantly to
the activation of renal pelvic sensory receptors by bradykinin,
likely via release of arachidonic acid.
Received 29 November 1994; accepted in final form 3 March 1995.
APS Manuscript Number R683-4.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 10 March 1995.