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Tachykinins and their receptors: contributions to physiological control and the mechanisms of disease.
Tachykinins (TACs) are characterized by pharmacological similarity to their endogenous inflammatory mediator, bradykinin, yet TACs are not of similar structure to that of bradykinin.
Effects of central administration of tachykinin receptor agonists and antagonists on plus-maze behavior in mice.
Primary afferent tachykinins are required to experience moderate to intense pain.
Airway neurogenic inflammation is caused by tachykinins released from sensory neuron peripheral nerve endings within the airways, and is characterized by plasma protein extravasation, airway smooth muscle contraction and increased secretion of mucus (25, 108).
The pharmacology of GR203040, a novel, potent and selective non-peptide tachykinin NK1 receptor antagonist.
Substance P (SP), a neuropeptide and member of the tachykinin family, has potent effects on airway smooth muscle tone, vascular permeability, and mucus secretion (Barnes et al.
Further evidence for the involvement of tachykinin receptor subtypes in formalin and capsaicin models of pain in mice.
Tachykinin peptides, receptors, and peptidases in airway disease.
Furthermore, elevated levels of sensory nerve-mediated tachykinin substance P were found in nasal lavage fluid (NAL) of patients with chronic cough and increased capsaicin cough sensitivity (Cho et al.
Tachykinin NK1 and receptor-mediated control of peristaltic propulsion in the guinea-pig small intestine in vivo.