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Sensory and Inflammatory Peptide Receptors in Airways
Published in Devendra K. Agrawal, Robert G. Townley, Inflammatory Cells and Mediators in Bronchial Asthma, 2020
SP is localized to unmyelinated sensory nerves (C-fibers) in airways.5–7 In rodents there is a rich innervation of SP-immunoreactive nerves which are found in close association with airway epithelium and sometimes penetrate the epithelial layer. In addition, SP-immunoreactive nerves are also seen in airway smooth muscle, around submucosal glands, around submucosal blood vessels, and in relation to parasympathetic ganglia. In human airways, SP innervation is much less prominent7 and in some studies has not been found.8 This may be related to the fact that human airways have usually been obtained at surgery for lung carcinoma from older smokers in whom these nerves may be depleted. Preliminary studies have shown that in asthmatic airways there may be a prominent SP innervation, suggesting that chronic inflammation may lead to proliferation of these nerves. Recently, three other tachykinins have been identified in the mammalian nervous system. Neurokinin A (NKA), which was previously known as substance K, is coded by the same gene as SP9 and is often colocalized with it in sensory nerves. NKA is localized to sensory nerves in animal and human airways.10 Neuropeptide K is an N-terminally extended form of NKA which is also coded by the same gene. NKB (previously known as neuromedin K) is localized predominantly to the brain and is coded by a separate gene.11 It has not yet been reported in the lung.
Postulated Physiological and Pathophysiological Roles on Motility
Published in Edwin E. Daniel, Neuropeptide Function in the Gastrointestinal Tract, 2019
Hans-Dieter Allescher, Sultan Ahmad
Recently, two novel mammalian tachykinins, neurokinin A (NKA) and neurokinin B (NKB), which are structurally related to kassinin, have been identified and isolated from the mammalian spinal cord.281–285 In addition, an N-terminally extended form of neurokinin A with 36 amino acids was isolated from the porcine brain and named neuropeptide K (NP-K).286 There is some evidence that additional, so far unidentified tachykinin-like peptides might be present.287–291 Substance P, neuropeptide K, neurokinin A, and neurokinin B have a common C-terminal amino acid sequence.
Role Of Neural Substance P And Coexisting Calcitonin Gene-Related Peptide (Cgrp) In Cardiovascular Function
Published in Geoffrey Burnstock, Susan G. Griffith, Nonadrenergic Innervation of Blood Vessels, 2019
The edema of the tracheal mucosa induced by vagal nerve stimulation and a variety of chemical irritants, such as ether, formalin, nicotine, and cigarette smoke, is absent in capsaicin-pretreated animals.52, 57 Furthermore, the tracheobronchial edema induced by cigarette smoke can be blocked by specific substance P antagonists.58 Some capsaicin-sensitive nerves in the airways thus seem to represent chemosensitive afferents which upon irritation can induce local edema and vasodilatation, probably through release of substance P or a related tachykinin (Figure 8).59 Also the other tachykinins — viz. neurokinin A, neuropeptide K, and eledoisin — induce protein extravasation as well as a fall in systemic blood pressure (Figure 9). With regard to the extravasation, eledoisin and substance P appear to be the most potent tachykinins.60 Indeed, there is reason to believe that these tachykinins are present in the same sensory neurons (Figure 10).
Decreased neurokinin B as a risk factor of functional hypothalamic amenorrhea
Published in Gynecological Endocrinology, 2023
Anna Szeliga, Agnieszka Podfigurna, Gregory Bala, Blazej Meczekalski
NKB belongs to the tachykinin family of proteins. They share a common C-terminal amino acid sequence (Phe-X-Gly-Leu-Met-NH2) and include substance P, neurokinin A, and NKB, as well as neuropeptide K, neuropeptide γ, and hemokinin-1 [2]. NKB mRNA-expressing neurons have been identified in both the basal forebrain and hypothalamus, mainly in the arcuate nucleus (ARCN) and the preoptic area (POA) but are also found in the septal and basal regions of Meynert, terminal striatum, amygdala, and neocortex [3]. Beyond humans, NKB-expressing neurons have also been found in the arcuate nucleus of monkeys, sheep, goats, and mice, indicating a high degree of homology of these nuclei between species [4–7].
The role of kisspeptin/neurokinin B/dynorphin neurons in pathomechanism of vasomotor symptoms in postmenopausal women: from physiology to potential therapeutic applications
Published in Gynecological Endocrinology, 2018
Anna Szeliga, Adam Czyzyk, Agnieszka Podfigurna, Andrea R. Genazzani, Alessandro D. Genazzani, Blazej Meczekalski
The NKB is a decapeptide and together with substance P, neurokinin A, neuropeptide K, neuropeptide ɣ, and hemokinin-1 belongs to the tachykinin family [40,41]. It is encoded by the TAC3 gene and is synthesized by KNDy neurons in the infundibular nucleus of the hypothalamus. The NKB binds to its receptor, NK3R, encoded by the TACR3 gene. With coaction of KISS1 and dynorphin, it is a major regulator of the GnRH secretion [42]. Its pulsatile secretion stimulates KISS1, and subsequently GnRH and LH secretion. NK3R is present not only on KNDy neurons, where NKB plays an autoregulatory role, but also in organs and tissues located outside the central nervous system such as uterus, intestines, placenta, and mesenteric vein. NK3R can be stimulated by other neuropeptides belonging to tachykinin family, when present in high concentration [43]. Observation of patients with TAC3 or TACR3 gene mutations provided more information about connection between reproductive axis and NKB. Patients with inactivating mutations in either TAC3 or TACR3 gene present decreased concentration of ovarian hormones, lack of pubertal development, and develop hypogonadotropic hypogonadism, whereas mutations leading to overactivation cause precocious puberty [25,44,45]. Administration of NKB in patients with TAC3 or TAC3R gene inactivating mutations restores pulsatile LH secretion and gonadal function confirming superior role of NKB in the regulation of gonadal function [46]. Nevertheless, NKB deficiency seems to be reversal after delayed puberty. This suggest that impairment in hypothalamic regulation of gonadal axis is not so severe as in the cases of KISS1 or KISS1R gene mutations [45].
Neurokinin receptor antagonism: a patent review (2014-present)
Published in Expert Opinion on Therapeutic Patents, 2020
Substance P (SP), hemokinin-1, neurokinin A (NKA), neurokinin B (NKB), neuropeptide K, eledoisin, ranakinin, and kassinin belong to the tachykinin family of peptides which, via the metabotropic neurokinin (NK)-1, NK-2 and NK-3 receptors, exert many physiological actions and are involved in many pathophysiological mechanisms (e.g. cancer, emesis, anxiety, depression, pain, alcohol addiction, inflammation, viral and bacterial infection, pruritus) [1–3].