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1 Department of Internal Medicine, Department of Veterans Affairs Medical Center, Iowa City; University of Iowa College of Medicine, Iowa City, Iowa 52242; and 2 Department of Neuroscience, Karolinska Institutet, S-171 77 Stockholm, Sweden
Nerve terminals containing
neuronal nitric oxide synthase (nNOS) are localized in the renal pelvic
wall where the sensory nerves containing substance P and calcitonin
gene-related peptide (CGRP) are found. We examined whether nNOS is
colocalized with substance P and CGRP. All renal pelvic nerve fibers
that contained nNOS-like immunoreactivity (-LI) also contained
substance P-LI and CGRP-LI. In anesthetized rats, renal pelvic
perfusion with the nNOS inhibitor
S-methyl-L-thiocitrulline (L-SMTC,
20 µM) prolonged the afferent renal nerve activity (ARNA) response to
a 3-min period of increased renal pelvic pressure from 5 ± 0.4 to
21 ± 2 min (P < 0.01, n = 14).
The magnitude of the ARNA response was unaffected by
L-SMTC. Similar effects were produced by
N
-nitro-L-arginine methyl ester
(L-NAME) but not D-NAME. Increasing renal
pelvic pressure produced similar increases in renal pelvic release of
substance P before and during L-SMTC, from 5.9 ± 1.4 to 13.6 ± 4.2 pg/min before and from 4.9 ± to 12.6 ± 2.7 pg/min during L-SMTC. L-SMTC also prolonged
the ARNA response to renal pelvic perfusion with substance P (3 µM)
from 1.2 ± 0.2 to 5.6 ± 1.1 min (P < 0.01, n = 9) without affecting the magnitude of the ARNA
response. In conclusion: activation of NO may function as an inhibitory
neurotransmitter regulating the activation of renal mechanosensory
nerve fibers by mechanisms related to activation of substance P receptors.
mechanosensory neurons; neuronal nitric oxide synthase; renal pelvis; afferent renal nerve activity; calcitonin gene-related peptide; dorsal root ganglion
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