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Abstract
The preprotachykinin-A gene-derived peptides substance (substance P; SP) and neurokinin
(NK) A are expressed in intrinsic enteric neurons, which supply all layers of the
gut, and extrinsic primary afferent nerve fibers, which innervate primarily the arterial
vascular system. The actions of tachykinins on the digestive effector systems are
mediated by three different types of tachykinin receptor, termed NK1, NK2 and NK3
receptors. Within the enteric nervous system, SP and NKA are likely to mediate, or
comediate, slow synaptic transmission and to modulate neuronal excitability via stimulation
of NK3 and NK1 receptors. In the intestinal mucosa, tachykinins cause net secretion
of fluid and electrolytes, and it appears as if SP and NKA play a messenger role in
intramural secretory reflex pathways. Secretory processes in the salivary glands and
pancreas are likewise influenced by tachykinins. The gastrointestinal arterial system
may be dilated or constricted by tachykinins, whereas constriction and an increase
in the vascular permeability are the only effects seen in the venous system. Various
gastrointestinal disorders are associated with distinct changes in the tachykinin
system, and there is increasing evidence that tachykinins participate in the hypersecretory,
vascular and immunological disturbances associated with infection and inflammatory
bowel disease. In a therapeutic perspective, it would seem conceivable that tachykinin
antagonists could be exploited as antidiarrheal, antiinflammatory and antinociceptive
drugs.