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1 Gastrointestinal Research Group, University of Calgary, Calgary, Alberta T2N 4N1; and 2 Gastrointestinal Diseases Research Unit, Queen's University, Kingston, Ontario, Canada K7L 5G2
This study characterized tachykinin-evoked
secretomotor responses in in vitro submucosal and mucosal-submucosal
preparations of the guinea pig ileum using combined intracellular and
Ussing chamber recording techniques. Superfusion of endogenous
tachykinins substance P (SP), neurokinin A (NKA), and neurokinin
B depolarized single submucosal neurons and evoked increased
short-circuit current (Isc) responses in
Ussing chamber preparations. The NK1-receptor agonist
[Sar9,Met(O2)11]SP
[50% effective concentration (EC50) = 2 nM] depolarized all submucosal neurons examined. The
NK3-receptor agonist
senktide (EC50 = 20 nM) depolarized ~50% of neurons examined, whereas the NK2-receptor agonist
[Ala5,
-Ala8]NKA-(4
10)
had no effect on membrane potential.
[Sar9,Met(O2)11]SP
and senktide evoked similar increases in
Isc that were
tetrodotoxin sensitive (91 and 100%, respectively) and were
selectively blocked by the NK1
antagonist CP-99,994 and the NK3
antagonist SR-142801, respectively. Capsaicin-evoked increases in
Isc were
significantly inhibited (54%, P < 0.05) by CP-99,994 but not by SR-142801. Neither antagonist inhibited
slow excitatory postsynaptic potentials. These findings suggest that
tachykinin-evoked secretion in guinea pig ileum is mediated by
NK1 and
NK3 receptors on submucosal
secretomotor neurons and that capsaicin-sensitive nerves release
tachykinin(s) that activate the
NK1 receptors.
substance P; ion transport; submucosal neurons; neurokinins; secretion
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