Regulatory role of tachykinins on intestinal propulsive activity

Abstract

The role of NK1, NK2, NK3 tachykinin receptors in subserving intestinal peristalsis has been reviewed referring mainly to the latest advances in this field. The most interesting and intriguing notion emerging from recent and ongoing studies is that tachykinins present in enteric neurons may modulate propulsive activity in an opposite manner, by enhancing or inhibiting peristalsis via each of the three distinct tachykinin receptors. These studies unveiled the complexity of tachykinergic control of the intestinal motility which is due to interaction of endogenous tachykinins with receptors located on ascending excitatory and descending inhibitory pathways and on smooth muscle cells. In fact, the type of tachykinergic modulation may depend on the amount of released peptides, on the site of the bulk of peptide release along the enteric motor pattern and, consequently, on the cellular location of the activated receptor, i.e. muscular or neuronal cells. Furthermore, in the case of activation of neuronally located tachykinin receptors, the effect of tachykinins may depend on the relatively functional predominance of excitatory or inhibitory neural circuits subserving peristalsis in different intestinal tracts. Our findings obtained in a simple isolated model represent a promising start for the understanding of the complex tachykinergic modulatory role of intestinal motility even though the function of tachykinins studied "in vivo" is certainly more complex than that studied "in vitro".