Tachykinins mediate a variety of physiological processes in the gastrointestinal, pulmonary and genito-urinary tract mainly through the stimulation of NK1 and NK2 receptors. Preclinical evidence obtained through the use of selective tachykinin receptor antagonists indicates that endogenous tachykinins are involved in augmented smooth muscle contraction, vasodilatation, chemotaxis and activation of immune cells, mucus secretion, water absorption/secretion. Recent evidence also suggests that endogenous tachykinins released at the peripheral level may play a role in visceral inflammation, hyperreflexia and hyperalgesia. Possible mechanisms underlying the stimulation of primary afferent neurons by tachykinins may involve a direct excitation of these neurons and the release of mediators which sensitise or stimulate sensory nerves. Tachykinin receptor antagonists could have a clinical utility in several human diseases such as irritable bowel syndrome, asthma, and in micturition disturbances characterized by a hyperactive bladder.
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