Tachykinin Receptors and their Antagonists
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Neurokinin B
Neurokinin A
Tachykinin receptor
The actions of mammalian tachykinins (substance P, substance K/neurokinin a, neuromedin K/neurokinin b) and non-mammalian tachykinins (eledoisin, kassinin, physalaemin) were compared on the rabbit pupillary sphincter. All acted as direct spasmogens with potencies in the order: eledoisin greater than physalaemin = neurokinin b = substance P greater than kassinin greater than neurokinin a. However, their actions could be divided into at least two categories on the basis of similar kinetics of contractions, differential sensitivity to the tachykinin antagonist (D-Arg1, D-Pro2, D-Trp7,9, Leu11) substance P and specific cross-protection against phenoxybenzamine inactivation by structurally related tachykinins. The relationship between these observations and the suggested "P" and "E" subtypes of tachykinin receptors is discussed.
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Tachykinins (also known as neurokinins) share a common C-terminal sequence, Phe-X-Gly-Leu-Met-NH2 (where X is Phe, Tyr, Val or Ile). Substance P was the first to be discovered and is the best characterised. Other tachykinins notable for their widespread distribution in mammalian tissues, including the peripheral and central nervous system, are neurokinins A and B. The biological actions of tachykinins are through G-protein linked receptors designated NK1, NK2 and NK3 and there has been an assumption that the preferred agonists were substance P, neurokinin A and neurokinin B respectively [1], [2]. However, the receptor selectivity of these peptides is relatively poor. There is a mismatch between tachykinin-containing neurones and fibres and their corresponding receptor in certain brain regions and this is particularly apparent in the case of neurokinin A since NK2 receptor expression appears to be extremely low in the adult mammalian nervous system [3]. A novel NK4 receptor has been proposed and it appears that there are two NK3 receptors designated A and B [4].
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