Renal sensory receptor activation causes prostaglandin dependent
release of substance p..
Kopp, Ulla C., Donna M. Farley, and Lori A. Smith.
Departments of Internal Medicine and Obstetrics/Gynecology,
University of Iowa College of Medicine and Department of Veterans
Affairs Medical Center, Iowa City, Iowa 52242
APStracts 2:0299R, 1995.
Renal mechanoreceptor (MR) activation by increased ureteral pressure
(UP) results in an increase in afferent renal nerve activity (ARNA)
that is blocked by substance P receptor blockade and prostaglandin
(PG) synthesis inhibition. To examine the interaction between
substance P and PGs, the release of substance P and PGE into the
renal pelvis was studied before and during renal pelvic perfusion
with indomethacin. Before indomethacin, UP increased ARNA 43+/-6% and
renal pelvic release of substance P from 11+/-3 to 29+/-8 pg/min and
PGE from 319+/-71 to 880+/-146 pg/min. Indomethacin blocked the
increases in ARNA and release of substance P and PGE produced by UP.
Time control experiments showed reproducible increases in ARNA and
release of substance P and PGE during UP. Mechanical stimulation of
the renal pelvic wall in vitro resulted in an increase in PGE
release, from 110+/-8 to 722+/-152 pg/min, that was abolished by
indomethacin, suggesting a de novo PGE synthesis. The data suggest
that UP results in a renal pelvic release of PGE which facilitates
the release of substance P and activation of renal pelvic MR.
Received 27 July 1995; accepted in final form 23 October 1995.
APS Manuscript Number R469-5.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 14 November 95