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Artykuły w czasopismach na temat „Tachykinins”

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Data publikacji: 4 czerwca 2021

Data aktualizacji: 25 lipca 2025

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1

López, B. Díaz, and L. Debeljuk. "Prenatal melatonin and its interaction with tachykinins in the hypothalamic - pituitary - gonadal axis." Reproduction, Fertility and Development 19, no. 3 (2007): 443. http://dx.doi.org/10.1071/rd06140.

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The pineal gland, through its hormone melatonin, influences the function of the hypothalamic–pituitary–gonadal axis. Tachykinins are bioactive peptides whose presence has been demonstrated in the pineal gland, hypothalamus, anterior pituitary gland and the gonads, in addition to other central and peripheral structures. Tachykinins have been demonstrated to influence the function of the hypothalamic–pituitary–gonadal axis, acting as paracrine factors at each of these levels. In the present review, we examine the available evidence supporting a role for melatonin in the regulation of reproductiv

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2

Fujii, K., H. Kohrogi, H. Iwagoe, et al. "Evidence that PGF2 alpha-induced contraction of isolated guinea pig bronchi is mediated in part by release of tachykinins." Journal of Applied Physiology 79, no. 5 (1995): 1411–18. http://dx.doi.org/10.1152/jappl.1995.79.5.1411.

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To investigate whether prostaglandin F2 alpha (PGF2 alpha) stimulates the release of tachykinins and whether the tachykinins play a role in the PGF2 alpha-induced bronchial contraction, we examined the contractile response to PGF2 alpha in the presence or absence of a neutral endopeptidase (NEP) inhibitor phosphoramidon in the guinea pig main bronchus in vitro. Because NEP effectively cleaves tachykinins, we hypothesized that the inhibition of NEP would enhance a PGF2 alpha-induced bronchial contraction if PGF2 alpha stimulates the release of tachykinins. Phosphoramidon significantly enhanced

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3

Payne, Catherine M., Caroline J. Heggie, David G. Brownstein, James P. Stewart, and John P. Quinn. "Role of Tachykinins in the Host Response to Murine Gammaherpesvirus Infection." Journal of Virology 75, no. 21 (2001): 10467–71. http://dx.doi.org/10.1128/jvi.75.21.10467-10471.2001.

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ABSTRACT Tachykinins function not only as neurotransmitters but also as immunological mediators. We used infection of tachykinin-deficient (PPT-A −/−) mice and wild-type controls with murine gammaherpesvirus to assess the role of tachykinins in the host response to a virus infection. Although infection was ultimately controlled in PPT-A −/− mice, there were higher titers of infectious virus in the lungs, accompanied by a more rapid influx of inflammatory cells. Clearance of latently infected cells from the spleen was also delayed. This is the first report of the direct influence of tachykinins

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4

Weinstock, J. V., and A. M. Blum. "Tachykinin production in granulomas of murine schistosomiasis mansoni." Journal of Immunology 142, no. 9 (1989): 3256–61. http://dx.doi.org/10.4049/jimmunol.142.9.3256.

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Abstract Preprotachykinins, the products of one gene, are the precursor molecules of three mammalian tachykinins called substance P (SP), substance K (SK), and neuropeptide K. An additional mammalian tachykinin, neurokinin B, has also been described. SP and possibly other tachykinins may modulate immunologic responses. Granulomas that form around parasite ova in murine schistosomiasis were examined for tachykinins. Tachykinins were extracted from granulomas by boiling or with detergent. Extracts examined by RIA and HPLC contained only immunoreactive SP. Granulomas were dispersed with collagena

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5

Culman, Juraj, and Thomas Unger. "Central tachykinins: mediators of defence reaction and stress reactions." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 885–91. http://dx.doi.org/10.1139/y95-122.

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The tachykinins substance P, neurokinin A, and neurokinin B are natural agonists for NK1, NK2, and NK3 receptors, respectively. Evidence from biochemical, neurophysiological, pharmacological, and molecular biology studies indicates that the tachykinin-containing pathways within the brain contribute to central cardiovascular and endocrine regulation and to the control of motor activity. The hypothalamus, which represents a site for the integration of central neuroendocrine and autonomic processes, is rich in tachykinin nerve endings and tachykinin receptors. Stimulation of periventricular or hy

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6

Weil, M., A. Itin, and E. Keshet. "A role for mesenchyme-derived tachykinins in tooth and mammary gland morphogenesis." Development 121, no. 8 (1995): 2419–28. http://dx.doi.org/10.1242/dev.121.8.2419.

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Tachykinin peptides such as substance P (SP) function as neurotransmitters and neuromodulators in the mammalian central and peripheral nervous systems. Here, we provide evidence that they may also play an important role in the morphogenesis of some nonneural organs where epithelial-mesenchymal interactions are involved. We show the following. (1) mRNA encoding tachykinin precursor proteins is expressed transiently in condensing mesenchyme during the development of mouse tooth germ, mammary gland, limb bud, external auditory meatus and genital tubercle. (2) In developing tooth germ and mammary

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7

Kagstrom, J., M. Axelsson, J. Jensen, A. P. Farrell, and S. Holmgren. "Vasoactivity and immunoreactivity of fish tachykinins in the vascular system of the spiny dogfish." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 270, no. 3 (1996): R585—R593. http://dx.doi.org/10.1152/ajpregu.1996.270.3.r585.

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Tachykinin control of gut blood flow (measured by pulsed Doppler technique), dorsal aortic pressure, and heart rate were studied in unrestrained spiny dogfish Squalus acanthias injected with the elasmobranch tachykinins scyliorhinin I and II (SCY I and SCY II), the trout tachykinins substance P (SP), and neurokinin A (NKA). Effects on somatic vasculature were measured by in vitro perfusion of the isolated tail. SCY I and trout SP produced hypotension due to a general vasodilation. This caused a transient increase in mesenteric blood flow and a prolonged increase in celiac blood flow. SCY II ca

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8

Jensen, J., K. R. Olson, and J. M. Conlon. "Primary structures and effects on gastrointestinal motility of tachykinins from the rainbow trout." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 265, no. 4 (1993): R804—R810. http://dx.doi.org/10.1152/ajpregu.1993.265.4.r804.

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Purification and structural characterization of tachykinins from rainbow trout (Oncorhynchus mykiss) intestine has demonstrated the presence of three different peptides related to the mammalian tachykinins: substance P, neurokinin A, and neuropeptide-gamma. The substance P- and the neurokinin A-related peptides present in the intestine are identical to the tachykinins previously isolated from the trout brain. The neuropeptide-gamma-related peptide (Ser-Ser-Ala-Asn-Pro-Gln-Ile-Thr-Arg-Lys-Arg-His-Lys-Ile-Asn-Ser-Phe- Val-Gly-Leu-Met-NH2), not previously identified in brain tissue, has the seque

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9

Cao, Thong, Norma P. Gerard, and Susan D. Brain. "Use of NK1knockout mice to analyze substance P-induced edema formation." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 277, no. 2 (1999): R476—R481. http://dx.doi.org/10.1152/ajpregu.1999.277.2.r476.

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The mechanisms involved in tachykinin-induced neurokinin-1 (NK1) receptor-mediated edema formation have been studied in anesthetized wild-type and NK1knockout mice. Intradermally injected substance P (30–300 pmol), NK1agonists septide (3–30 pmol) and GR-73632 (3–30 pmol), and the mast cell-degranulating agent, compound 48/80 induced dose-dependent edema in wild-type skin, measured by the accumulation of intravenously injected125I-labeled albumin. Septide was 3–10× more potent than substance P. The tachykinins were inactive in knockout mice, but compound 48/80 induced a significantly greater ed

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10

Williams, Ronald, Xiaoyan Zou та Gary W. Hoyle. "Tachykinin-1 receptor stimulates proinflammatory gene expression in lung epithelial cells through activation of NF-κB via a Gq-dependent pathway". American Journal of Physiology-Lung Cellular and Molecular Physiology 292, № 2 (2007): L430—L437. http://dx.doi.org/10.1152/ajplung.00475.2005.

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The respiratory tract is innervated by irritant-responsive sensory nerves, which, on stimulation, release tachykinin neuropeptides in the lung. Tachykinins modulate inflammatory responses to injury by binding to tachykinin (neurokinin) receptors present on various pulmonary cell types. In the present study, the activation of the proinflammatory transcription factor NF-κB in lung epithelial cells was investigated as a mechanism by which tachykinins stimulate inflammatory processes. In A549 human lung epithelial cells transfected with the tachykinin-1 receptor (Tacr1), treatment with the Tacr1 l

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11

Pérez, Carolina Thörn, Russell H. Hill, and Sten Grillner. "Endogenous Tachykinin Release Contributes to the Locomotor Activity in Lamprey." Journal of Neurophysiology 97, no. 5 (2007): 3331–39. http://dx.doi.org/10.1152/jn.01302.2006.

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Tachykinins are present in lamprey spinal cord. The goal of this study was to investigate whether an endogenous release of tachykinins contributes to the activity of the spinal network generating locomotor activity. The locomotor network of the isolated lamprey spinal cord was activated by bath-applied N-methyl-d-aspartate (NMDA) and the efferent activity recorded from the ventral roots. When spantide II, a tachykinin receptor antagonist, was bath-applied after reaching a steady-state burst frequency (>2 h), it significantly lowered the burst rate compared with control pieces from the same

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12

Maggi, C. A. "Tachykinins, tachykinin receptors and airways pathophysiology." Pharmacological Research 26 (September 1992): 7. http://dx.doi.org/10.1016/1043-6618(92)90726-r.

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13

Goto, Tetsuya, and Teruo Tanaka. "Tachykinins and tachykinin receptors in bone." Microscopy Research and Technique 58, no. 2 (2002): 91–97. http://dx.doi.org/10.1002/jemt.10123.

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14

Leon, Silvia, and Víctor M. Navarro. "Novel Biology of Tachykinins in Gonadotropin-Releasing Hormone Secretion." Seminars in Reproductive Medicine 37, no. 03 (2019): 109–18. http://dx.doi.org/10.1055/s-0039-3400252.

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AbstractThe tachykinin family of peptides, composed of the neurokinins A and B (NKA, NKB) and substance P are involved in the central control of gonadotropin-releasing hormone (GnRH) release through a variety of neuronal circuitries that mediate the activation of Kiss1 neurons and the synchronization of their activity within the arcuate nucleus. The major outcome of this role is the precise regulation of the pulsatile pattern of GnRH release. In addition, tachykinins are involved in the maturation of the reproductive axis by determining the optimal timing of puberty onset, as well as in the ti

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15

Graham, Gwenda J., Joanne M. Stevens, Nigel M. Page, et al. "Tachykinins regulate the function of platelets." Blood 104, no. 4 (2004): 1058–65. http://dx.doi.org/10.1182/blood-2003-11-3979.

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AbstractEvidence has been mounting for peripheral functions for tachykinins, a family of neuropeptides including substance P (SP), neurokinin A, and neurokinin B, which are recognized for their roles in the central and peripheral nervous system. The recent discovery of 4 new members of this family, the endokinins (EKA, B, C, and D), which are distributed peripherally, adds support to the notion that tachykinins have physiologic/endocrine roles in the periphery. In the present study we report a fundamental new function for tachykinins in the regulation of platelet function. We show that SP stim

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16

Chang, Yingzi, Donald B. Hoover, and John C. Hancock. "Endogenous tachykinins cause bradycardia by stimulating cholinergic neurons in the isolated guinea pig heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 278, no. 6 (2000): R1483—R1489. http://dx.doi.org/10.1152/ajpregu.2000.278.6.r1483.

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The purpose of this study was to determine if endogenous tachykinins can cause bradycardia in the isolated perfused guinea pig heart through stimulation of cholinergic neurons. Capsaicin was used to stimulate release of tachykinins and calcitonin gene-related peptide (CGRP) from cardiac afferents. A bolus injection of 100 nmol capsaicin increased heart rate by 26 ± 7% from a baseline of 257 ± 14 beats/min ( n = 6, P < 0.01). This positive chronotropic response was converted to a minor bradycardic effect in hearts with 1 μM CGRP-(8—37) present to block CGRP receptors. The negative chronotrop

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17

Hamel, R., A. W. Ford-Hutchinson, C. Blazejczak, and A. Van Den Brekel. "Tachykinin involvement in cutaneous anaphylaxis in the guinea pig." Canadian Journal of Physiology and Pharmacology 66, no. 11 (1988): 1361–67. http://dx.doi.org/10.1139/y88-223.

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Permeability changes in the guinea-pig skin following intradermal (i.d.) injection of tachykinin agonists or antigen were monitored through the extravasation of 99mTc-labelled human serum albumin and blood flow changes through the accumulation of 51Cr-labelled microspheres. A variety of synthetic and natural tachykinins, including substance P and neurokinins A and B, were shown to be potent inducers of permeability changes. Neurokinins A and B, but not substance P, were also shown to be apparent vasoconstrictor agents. Permeability responses in sensitized guinea pigs to i.d. injection of antig

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18

Cook, G. A., D. Elliott, A. Metwali, et al. "Molecular evidence that granuloma T lymphocytes in murine schistosomiasis mansoni express an authentic substance P (NK-1) receptor." Journal of Immunology 152, no. 4 (1994): 1830–35. http://dx.doi.org/10.4049/jimmunol.152.4.1830.

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Abstract Murine Schistosomiasis mansoni is a parasitic disease in which granulomas develop around the schistosome ova that lodge in the liver and intestines of the host. The granuloma eosinophils make substance P (SP), a cytokine with immunoregulatory properties. Within the granuloma SP can modulate IFN-gamma production through interaction with a substance P-like receptor. SP belongs to a family of hormones called tachykinins. Three mammalian tachykinins are SP, neurokinin A (substance K), and neurokinin B (neuromedin K). In humans and rats, there are at least three distinct tachykinin recepto

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19

Patak, Eva, M. Luz Candenas, Jocelyn N. Pennefather, et al. "Tachykinins and tachykinin receptors in human uterus." British Journal of Pharmacology 139, no. 3 (2003): 523–32. http://dx.doi.org/10.1038/sj.bjp.0705279.

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Takano, Yukio, Ryo Saito, Akira Nagashima, Shigeyuki Nonaka, and Hiro-o. Kamiya. "TACHYKININ RECEPTOR SUBTYPE: CARDIOVASCULAR ROLES OF TACHYKININS." Japanese Journal of Pharmacology 52 (1990): 38. http://dx.doi.org/10.1016/s0021-5198(19)54985-x.

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Pennefather, Jocelyn N., Alessandro Lecci, M. Luz Candenas, Eva Patak, Francisco M. Pinto, and Carlo Alberto Maggi. "Tachykinins and tachykinin receptors: a growing family." Life Sciences 74, no. 12 (2004): 1445–63. http://dx.doi.org/10.1016/j.lfs.2003.09.039.

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Parker, D., and S. Grillner. "Tachykinin-mediated modulation of sensory neurons, interneurons, and synaptic transmission in the lamprey spinal cord." Journal of Neurophysiology 76, no. 6 (1996): 4031–39. http://dx.doi.org/10.1152/jn.1996.76.6.4031.

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1. Tachykinin-like immunoreactivity is found in the dorsal roots, dorsal horn, and dorsal column of the lamprey. The effect of tachykinins on sensory processing was examined by recording intracellularly from primary sensory dorsal cells and second-order spinobulbar giant interneurons. Modulation of synaptic transmission was examined by making paired recordings from dorsal cells and giant interneurons, or by eliciting compound depolarizations in the giant interneurons by stimulating the dorsal root or dorsal column. 2. Bath application of tachykinins depolarized the dorsal cells. This effect wa

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23

Blum, A. M., A. Metwali, G. Cook, R. C. Mathew, D. Elliott, and J. V. Weinstock. "Substance P modulates antigen-induced, IFN-gamma production in murine Schistosomiasis mansoni." Journal of Immunology 151, no. 1 (1993): 225–33. http://dx.doi.org/10.4049/jimmunol.151.1.225.

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Abstract In murine Schistosomiasis mansoni, granuloma eosinophils make SP. We investigated whether SP affects lymphokine secretion in murine schistosomiasis. SP at &gt; or = 10(-10) M, and other tachykinins at much higher concentrations, substantially increased IFN-gamma secretion from spleen or granuloma inflammatory cells primed in vitro by suboptimal stimulatory concentrations of egg Ag or mitogen. Cells receiving maximal antigenic or mitogenic stimulation were affected marginally. Also, tachykinins induced no IFN-gamma from resting cells receiving no Ag or mitogen stimulation. There ar

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Vannucchi, Maria Giuliana, and Stefano Evangelista. "Neurokinin receptors in the gastrointestinal muscle wall: cell distribution and possible roles." BioMolecular Concepts 4, no. 3 (2013): 221–31. http://dx.doi.org/10.1515/bmc-2013-0001.

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AbstractThe neurokinin receptors are G-protein-linked receptors; three distinct molecules, called neurokinin-1, neurokinin-2, and neurokinin-3 receptors, have been identified. Their physiological ligands are the tachykinins, which, in the mammalian gut, correspond to substance P, neurokinin A, and neurokinin B. In this apparatus, the main source of tachykinins is represented by intrinsic neurons located either in the myenteric plexus and projecting mainly to the muscle coat, or in the submucous plexus and projecting to the mucosa and submucosal blood vessels. The availability of specific antib

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Barber, W. D., G. D. Stevenson, and T. F. Burks. "Tachykinins: local gastric effects and brain stem responses." American Journal of Physiology-Gastrointestinal and Liver Physiology 252, no. 3 (1987): G365—G373. http://dx.doi.org/10.1152/ajpgi.1987.252.3.g365.

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The gastric motor or mechanical effects of a group of peptides, the tachykinins, were evaluated in anesthetized cats to determine the relationship between local motor events and brain stem neurons that regulate gastric activity. The peptides evaluated were substance P, physalaemin, and eledoisin. The tachykinin-induced gastric changes were dose related and were characterized by initial distention-sustained contraction-late distention phases. At lower doses distention was the dominant effect with a sustained contraction-late distention response appearing as the dose increased. The sustained con

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Souquet, J. C., J. R. Grider, K. N. Bitar, and G. M. Makhlouf. "Receptors for mammalian tachykinins on isolated intestinal smooth muscle cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 249, no. 4 (1985): G533—G538. http://dx.doi.org/10.1152/ajpgi.1985.249.4.g533.

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The existence of receptors for three mammalian tachykinins, substance P (SP), substance K (SK), and neuromedin K (NK), was examined in smooth muscle cells, isolated separately from the longitudinal and circular muscle layers of guinea pig ileum. Tachykinin receptors capable of mediating contraction were present in muscle cells from both layers. The receptors were selectively blocked by the tachykinin antagonist [D-Pro2, D-Trp7,9]substance P but not by muscarinic, gastrin/cholecystokinin, or opiate antagonists (0.3 nM atropine, 1 mM proglumide, and 0.3 nM naloxone, respectively). The rank order

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Von Essen, S. G., S. I. Rennard, D. O'Neill, et al. "Bronchial epithelial cells release neutrophil chemotactic activity in response to tachykinins." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 2 (1992): L226—L231. http://dx.doi.org/10.1152/ajplung.1992.263.2.l226.

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The purpose of this study was to determine whether substance P (SP), neurokinin A (NKA), and neurokinin B (NKB) induce the release of neutrophil chemotactic activity (NCA) from bovine bronchial epithelial cells (BBEC) and whether neutral endopeptidase (NEP), a membrane-bound metalloenzyme that hydrolyzes tachykinins, modulates these effects. BBEC monolayers were exposed to SP, NKA, and NKB in the absence or presence of phosphoramidon (10(-6) M), a selective NEP inhibitor, for 72 h. Using a modified blind-well in vitro neutrophil chemotaxis assay, we found that tachykinin-exposed BBEC culture s

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Stroff, T., S. Plate, J. S. Ebrahim, K. H. Ehrlich, M. Respondek, and B. M. Peskar. "Tachykinin-induced increase in gastric mucosal resistance: role of primary afferent neurons, CGRP, and NO." American Journal of Physiology-Gastrointestinal and Liver Physiology 271, no. 6 (1996): G1017—G1027. http://dx.doi.org/10.1152/ajpgi.1996.271.6.g1017.

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The tachykinins [Ala5,beta-Ala8]neurokinin A-(4-10) -[Ala5,beta-Ala8]NKA-(4-10) inverted question mark and NKA-(4-10) dose dependently protected against ethanol-induced gastric mucosal damage in rats (half-maximal inhibitory dose, 46 and 48 nmol/kg, respectively). These effects were abolished by primary afferent nerve denervation, calcitonin gene-related peptide (CGRP) immunoneutralization, the CGRP receptor antagonist human (h) hCGRP-(8-37), and inhibition of nitric oxide (NO) biosynthesis by NG-nitro-L-arginine methyl ester. Tachykinin-induced protection occurred despite marked depression of

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Couture, Réjean, Pierre Picard, Philippe Poulat, and Alexandre Prat. "Characterization of the tachykinin receptors involved in spinal and supraspinal cardiovascular regulation." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 892–902. http://dx.doi.org/10.1139/y95-123.

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The pharmacological characterization of the tachykinin receptors involved in spinal and supraspinal cardiovascular regulation is reviewed in this report. In conscious rats, substance P (SP), neurokinin A (NKA), neurokinin B (NKB), neuropeptide K (NPK), and neuropeptide γ (NPγ) were injected either intrathecally (i.t.) or intracerebroventricularly (i.c.v.), and their effects were assessed on mean arterial blood pressure (MAP) and heart rate (HR). Moreover, selective antagonists for NK1 ((±)-CP-96345 and RP-67580), NK2 (SR-48968), and NK3 (R-486) receptors were tested against the agonists. I.t.

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Joos, GF, PR Germonpre, JC Kips, RA Peleman, and RA Pauwels. "Sensory neuropeptides and the human lower airways: present state and future directions." European Respiratory Journal 7, no. 6 (1994): 1161–71. http://dx.doi.org/10.1183/09031936.94.07061161.

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The sensory neuropeptides, substance P and neurokinin A, are present in human airway nerves, beneath and within the epithelium, around blood vessels and submucosal glands, and within the bronchial smooth muscle layer. Studies on autopsy tissue, bronchoalveolar lavage and sputum suggest that in asthma the substance P content of the airways may be increased. Neurokinin A is a more potent bronchoconstrictor than substance P. Asthmatics are hyperresponsive to neurokinin A and substance P. The neuropeptide degrading enzyme, neutral endopeptidase is present in the airways and is involved in the degr

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Almeida, T. A., J. Rojo, P. M. Nieto, et al. "Tachykinins and Tachykinin Receptors: Structure and Activity Relationships." Current Medicinal Chemistry 11, no. 15 (2004): 2045–81. http://dx.doi.org/10.2174/0929867043364748.

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Geppetti, Pierangelo, Claude Bertrand, Fabio M. L. Ricciardolo, and Jay A. Nadei. "New aspects on the role of kinins in neurogenic inflammation." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 843–47. http://dx.doi.org/10.1139/y95-115.

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The inflammatory response to injury consists of the activation of several protective mechanisms involving different cellular systems. Among the mechanisms and systems that exert their effects rapidly, peptide transmitters released from peripheral endings of primary sensory neurons (evoking neurogenic inflammation) play a major role in the response to tissue injury. Noxious stimuli may directly activate sensory nerves to release proinflammatory neuropeptides. More recently, evidence has accumulated suggesting that indirect mechanisms leading to sensory neuropeptide release are also activated in

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EL-AGNAF, Omar M. A., G. Brent IRVINE, Geraldine FITZPATRICK, W. Kenneth GLASS та David J. S. GUTHRIE. "Comparative studies on peptides representing the so-called tachykinin-like region of the Alzheimer Aβ peptide [Aβ(25–35)]". Biochemical Journal 336, № 2 (1998): 419–27. http://dx.doi.org/10.1042/bj3360419.

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In an attempt to answer the question of whether or not the so-called tachykinin-like region of the Alzheimer β-amyloid protein [Aβ(25–35)] can act as a tachykinin, the sequences Aβ(25–35), Aβ(25–35)amide and their norleucine-35 and phenylalanine-31 analogues were synthesized. These peptides were examined with ligand binding studies, electron microscopy, CD and NMR. In all cases some differences were found between the Aβ(25–35) analogue and the corresponding Phe31 peptide. In addition, in ligand displacement studies on tachykinin NK1 receptors, only the Phe31 analogue showed activity comparable

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Rogers, Duncan F. "Neurokinin receptors subserving airways secretion." Canadian Journal of Physiology and Pharmacology 73, no. 7 (1995): 932–39. http://dx.doi.org/10.1139/y95-129.

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Mucus secretion can be induced in the airways by activation of nerves. The principal mechanism mediating neurogenic mucus secretion is cholinergic. However, a small but significant secretory response remains after adrenoceptor and cholinoceptor blockade. The identity of this nonadrenergic, noncholinergic (NANC) neural mechanism is unclear but includes an orthodromic pathway and a capsaicin-sensitive "sensory-efferent" (or "local effector") pathway. The orthodromic pathway comprises cholinergic nerves (and to a much lesser extent adrenergic nerves) in which neuropeptides, including vasoactive i

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Maggio, J. E. "Tachykinins." Annual Review of Neuroscience 11, no. 1 (1988): 13–28. http://dx.doi.org/10.1146/annurev.ne.11.030188.000305.

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Mukda, S., B. Chetsawang, P. Govitrapong, P. T. Schmidt, A. Hay-Schmidt, and M. Møller. "Tachykinins and tachykinin-receptors in the rat pineal gland." European Journal of Neuroscience 21, no. 10 (2005): 2743–51. http://dx.doi.org/10.1111/j.1460-9568.2005.04088.x.

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Candenas, Luz, Alessandro Lecci, Francisco M. Pinto, Eva Patak, Carlo Alberto Maggi, and Jocelyn N. Pennefather. "Tachykinins and tachykinin receptors: effects in the genitourinary tract." Life Sciences 76, no. 8 (2005): 835–62. http://dx.doi.org/10.1016/j.lfs.2004.10.004.

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Manning, Brian P., and Gary M. Mawe. "Tachykinins mediate slow excitatory postsynaptic transmission in guinea pig sphincter of Oddi ganglia." American Journal of Physiology-Gastrointestinal and Liver Physiology 281, no. 2 (2001): G357—G364. http://dx.doi.org/10.1152/ajpgi.2001.281.2.g357.

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Intracellular recording techniques were used to test whether tachykinins could be mediators of slow excitatory postsynaptic potentials (EPSPs) in guinea pig sphincter of Oddi (SO) ganglia. Application of the tachykinin substance P (SP) onto SO neurons caused a prolonged membrane depolarization that was reminiscent of the slow EPSP in these cells. Pressure ejection of the neurokinin 3 (NK3) receptor-specific agonist senktide caused a similar depolarization; however, no responses were detected on application of NK1 or NK2 receptor agonists. The NK3 receptor antagonist SR-142801 (100 nM) signific

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Figini, M., C. Emanueli, E. F. Grady, et al. "Substance P and bradykinin stimulate plasma extravasation in the mouse gastrointestinal tract and pancreas." American Journal of Physiology-Gastrointestinal and Liver Physiology 272, no. 4 (1997): G785—G793. http://dx.doi.org/10.1152/ajpgi.1997.272.4.g785.

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Neurogenic inflammation is mediated by release of tachykinins from sensory nerves, which stimulate plasma extravasation from postcapillary venules. Because there are conflicting results regarding the importance of neurogenic inflammation in the gastrointestinal tract, we quantified plasma extravasation using Evans blue and identified sites of the leak using Monastral blue in the mouse. Substance P and bradykinin stimulated extravasation from postcapillary venules in the stomach, small and large intestine, pancreas, urinary bladder, trachea, and skin by two- to sevenfold by interacting with NK1

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Lee, H. K., C. W. Shuttleworth, and K. M. Sanders. "Tachykinins activate nonselective cation currents in canine colonic myocytes." American Journal of Physiology-Cell Physiology 269, no. 6 (1995): C1394—C1401. http://dx.doi.org/10.1152/ajpcell.1995.269.6.c1394.

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The mechanism of tachykinin-induced excitation was studied in isolated colonic muscle cells and intact muscle strips. In whole cell voltage-clamp studies performed at 33 degrees C, neurokinin A (NKA) and substance P (SP) reduced L-type Ca2+ current. NKA and SP activated a cationic current that reversed near 0 mV. This current (INKA or ISP, respectively) had properties similar to the acetylcholine (ACh)-activated nonselective cation conductance (IACh), activated by muscarinic stimulation in other gastrointestinal smooth muscle cells. INKA and ISP were decreased when external Na+ was reduced. In

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Garland, A., J. E. Jordan, D. W. Ray, S. M. Spaethe, L. Alger, and J. Solway. "Role of eicosanoids in hyperpnea-induced airway responses in guinea pigs." Journal of Applied Physiology 75, no. 6 (1993): 2797–804. http://dx.doi.org/10.1152/jappl.1993.75.6.2797.

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Guinea pigs mechanically hyperventilated with dry gas exhibit hyperpnea-induced bronchoconstriction (HIB) and hyperpnea-induced bronchovascular hyperpermeability (HIBVH). Tachykinins released from airway C-fiber neurons are the central mediators of guinea pig HIB but play only a contributory role in HIBVH. Recent studies suggest that eicosanoid mediators can provoke bronchoconstriction and bronchovascular hyperpermeability, are released by dry gas hyperpnea, and can themselves elicit or modulate tachykinin release. We therefore hypothesized that eicosanoids may participate in HIB and/or HIBVH.

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Grundy, Luke, Russ Chess-Williams, Stuart M. Brierley, et al. "NKA enhances bladder-afferent mechanosensitivity via urothelial and detrusor activation." American Journal of Physiology-Renal Physiology 315, no. 4 (2018): F1174—F1185. http://dx.doi.org/10.1152/ajprenal.00106.2018.

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Tachykinins are expressed within bladder-innervating sensory afferents and have been shown to generate detrusor contraction and trigger micturition. The release of tachykinins from these sensory afferents may also activate tachykinin receptors on the urothelium or sensory afferents directly. Here, we investigated the direct and indirect influence of tachykinins on mechanosensation by recording sensory signaling from the bladder during distension, urothelial transmitter release ex vivo, and direct responses to neurokinin A (NKA) on isolated mouse urothelial cells and bladder-innervating DRG neu

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Tepper, J. S., D. L. Costa, S. Fitzgerald, D. L. Doerfler, and P. A. Bromberg. "Role of tachykinins in ozone-induced acute lung injury in guinea pigs." Journal of Applied Physiology 75, no. 3 (1993): 1404–11. http://dx.doi.org/10.1152/jappl.1993.75.3.1404.

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To examine the hypothesis that the acute reversible changes caused by ozone (O3) exposure are mediated by tachykinin release, guinea pigs were depleted of tachykinins by use of repeated capsaicin (CAP) injections before O3 exposure in an attempt to prevent O3-induced functional changes. Unexpectedly, CAP pretreatment caused divergent results in the functional responses to O3. Ventilatory measurements obtained from CAP-pretreated O3-exposed (CAP-O3) animals were exacerbated rather than diminished compared with the effects of O3 alone. Similarly, lavage fluid protein accumulation was enhanced in

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Ribeiro, J. M. "Characterization of a vasodilator from the salivary glands of the yellow fever mosquito Aedes aegypti." Journal of Experimental Biology 165, no. 1 (1992): 61–71. http://dx.doi.org/10.1242/jeb.165.1.61.

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Salivary gland homogenates and oil-induced saliva of the mosquito Aedes aegypti dilate the rabbit aortic ring and contract the guinea pig ileum. The vasodilatory activity is endothelium-dependent, heat-stable, sensitive to both trypsin and chymotrypsin treatments, and both smooth muscle activities cross-desensitize to the tachykinin peptide substance P. Both bioactivities co-elute when salivary gland homogenates are fractionated by reversed-phase HPLC. Molecular sieving chromatography indicates a relative molecular mass of 1400. A monoclonal antibody specific to the carboxy terminal region of

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Kawano, O., H. Kohrogi, T. Yamaguchi, S. Araki, and M. Ando. "Neutral endopeptidase inhibitor potentiates allergic bronchoconstriction in guinea pigs in vivo." Journal of Applied Physiology 75, no. 1 (1993): 185–90. http://dx.doi.org/10.1152/jappl.1993.75.1.185.

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To determine whether endogenous tachykinins are released in allergic airway response to contribute to bronchoconstriction and whether neutral endopeptidase (NEP), which effectively cleaves tachykinins, modulates that bronchoconstriction, we studied the effects of the NEP inhibitor phosphoramidon on bronchoconstriction induced by allergic response in anesthetized guinea pigs. We mechanically ventilated the guinea pigs sensitized with ovalbumin (OVA) in a bodyplethysmograph and measured the pulmonary resistance (RL). We exposed the sensitized guinea pigs to doubling concentrations of OVA aerosol

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Kinberg, Kirk, and Roger H. Kobayashi. "ACROLEIN INCREASES AIRWAY SENSITIVITY TO SUBSTANCE P AND DECREASES NEP ACTIVITY IN GUINEA PIGS." Pediatrics 94, no. 2 (1994): 258. http://dx.doi.org/10.1542/peds.94.2.258.

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Purpose of the Study. Airway hyper-responsiveness is a consistent observation seen in asthmatic patients. In asthma, inflammatory cellular influx and mediator release results in epithelial damage, vascular leak, and alterations in mucus production and secretion. Studies suggest that C-fibers which innervate airway epithelium may be more densely packed with substance P in asthmatic patients than in normal subjects. Damage to the epithelium may increase stimulation of the C-fibers and subsequent tachykinin release including substance P. Tachykinins are metabolized by neutral endopeptidase (NEP)

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Thörn Pérez, Carolina, Russell H. Hill, Abdeljabbar El Manira, and Sten Grillner. "Endocannabinoids Mediate Tachykinin-Induced Effects in the Lamprey Locomotor Network." Journal of Neurophysiology 102, no. 3 (2009): 1358–65. http://dx.doi.org/10.1152/jn.00294.2009.

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The spinal network underlying locomotion in lamprey is composed of excitatory and inhibitory interneurons mediating fast ionotropic action. In addition, several modulator systems are activated as locomotion is initiated, including the tachykinin system and the metabotropic glutamate receptor 1 (mGluR1), the latter operating partially via the endocannabinoid system. The effects of mGluR1 agonists and tachykinins resemble each other. Like mGluR1 agonists, the tachykinin substance P accelerates the burst rate and reduces the crossed inhibition in an activity-dependent fashion. The present study t

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Hanley, Michael R. "Mixed tachykinins." Nature 320, no. 6057 (1986): 26. http://dx.doi.org/10.1038/320026a0.

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CULMAN, JURAJ, KEIICHI ITOI, and THOMAS UNGER. "Hypothalamic Tachykinins." Annals of the New York Academy of Sciences 771, no. 1 Stress (1995): 204–18. http://dx.doi.org/10.1111/j.1749-6632.1995.tb44682.x.

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Noveral, J. P., and M. M. Grunstein. "Tachykinin regulation of airway smooth muscle cell proliferation." American Journal of Physiology-Lung Cellular and Molecular Physiology 269, no. 3 (1995): L339—L343. http://dx.doi.org/10.1152/ajplung.1995.269.3.l339.

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The tachykinins, substance P (SP) and neurokinins A (NKA) and B (NKB), have been identified in the respiratory tract and implicated in mediating neurogenic inflammation of the airways. To the extent that these neuropeptides may be involved in the pathogenesis of asthma, a condition associated with hyperplasia of airway smooth muscle (ASM), we examined the mitogenic effects and mechanisms of action of tachykinins in cultured rabbit ASM cells. SP was found to elicit dose-dependent (10(-14) to 10(-4) M) stimulation of ASM cell proliferation, with a mean (+/- SE) maximal increase in cell number of

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