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Department of Internal Medicine, Department of Veterans Affairs Medical Center and University of Iowa College of Medicine, Iowa City, Iowa 52242
Activation
of renal pelvic sensory nerves by increased pelvic pressure results in
a renal pelvic release of substance P that is dependent on intact
prostaglandin synthesis. An isolated renal pelvic wall preparation was
used to examine whether PGE2
increases the release of substance P from renal pelvic sensory nerves
and by what mechanisms. The validity of the model was tested by
examining whether 50 mM KCl increased substance P release from the
pelvic wall. Fifty millimolar KCl produced an increase in substance P release, from 9.6 ± 1.6 to 26.8 ± 4.0 pg/min,
P < 0.01, that was blocked by the
L-type calcium blocker verapamil (10 µM).
PGE2 (0.14 µM) increased the
release of substance P from the pelvic wall from 8.9 ± 0.9 to 20.6 ± 3.3 pg/min, P < 0.01. PGE2 failed to increase substance
P release in a calcium-free medium. The PGE2-induced substance P release
was blocked by the N-type calcium blocker 
-conotoxin (0.1 µM) but
was unaffected by verapamil. In conclusion,
PGE2 increases the release of
substance P from renal pelvic sensory nerves by a calcium-dependent
mechanism that requires influx of calcium via N-type calcium channels.
-conotoxin; verapamil; potassium chloride-mediated neuropeptide
release; prostaglandin E2
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