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Departments of 1 Pharmacology and 2 Anesthesiology, The Ohio State University, Columbus, Ohio 43210
The role of
adenosine A1 receptors (A1R) in reflex-evoked
short-circuit current
(Isc)
indicative of chloride secretion was studied in the guinea pig colon.
The A1R antagonist
8-cyclopentyltheophylline (CPT) enhanced reflex-evoked
Isc. Adenosine
deaminase and the nucleoside transport inhibitor
S-(4-nitrobenzyl)-6-thioinosine enhanced and reduced reflex-induced
Isc,
respectively. The A1R agonist
2-chloro-N6-cyclopentyladenosine
(CCPA) inhibited reflex-evoked
Isc at nanomolar concentrations, and its action was antagonized by CPT. In the presence
of either
N-acetyl-5-hydroxytryptophyl-5-hydroxytryptophan amide to block the 5-hydroxytryptamine (5-HT)-mediated pathway or
piroxicam to block the prostaglandin-mediated pathway, CCPA reduced the
residual reflex-evoked
Isc. CCPA reduced
the response to a 5-HT pulse without affecting the
tetrodotoxin-insensitive Isc responses to
carbachol or forskolin. Immunoreactivity for A1R was detected in the membrane
(10% of neurons) and cytoplasm (90% of neurons) of neural protein
gene product 9.5-immunoreactive (or S-100-negative) submucosal neurons,
in glia, and in the muscularis mucosa.
A1R immunoreactivity in a majority
of neurons remained elevated in the cytoplasm despite preincubation
with adenosine deaminase or CPT.
A1R immunoreactivity
colocalized in synaptophysin-immunoreactive presynaptic varicose nerve
terminals. The results indicate that endogenous adenosine binding to
high-affinity A1R on
submucosal neurons acts as a physiological brake to suppress
reflex-evoked Isc
indicative of chloride secretion.
5-hydroxytryptamine; prostaglandin; submucous plexus; chloride secretion
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