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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 reproductive functions, the possible role of tachykinins in pineal function and the possible interactions between melatonin and tachykinins in the hypothalamic–pituitary–gonadal axis. Evidence is presented showing that melatonin, given to pregnant rats, influences the developmental pattern of tachykinins in the hypothalamus and the anterior pituitary gland of the offspring during postnatal life. In the gonads, the effects of melatonin on the tachykinin developmental pattern were rather modest. In particular, in the present review, we have included a summary of our own work performed in the past few years on the effect of melatonin on tachykinin levels in the hypothalamic–pituitary–gonadal axis.
2

Fujii, K., H. Kohrogi, H. Iwagoe, J. Hamamoto, N. Hirata, T. Yamaguchi, O. Kawano, and M. Ando. "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 (November 1, 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 the concentration-response curve to PGF2 alpha. And it also significantly enhanced 10(-5) M PGF2 alpha-induced contraction. The enhancement was significantly attenuated in tissues where the tachykinins had been depleted by treatment with capsaicin. Furthermore, the enhancement of contraction was also significantly attenuated in the presence of tachykinin antagonist FK-224 (10(-5) M). Tetrodotoxin, a sodium-channel blocker that blocks nerve conduction, did not affect the enhancement. From these results we conclude that 1) PGF2 alpha causes the release of tachykinin-like substances, 2) these substances play a role in bronchial contraction in tissues where NEP activity is inhibited, and 3) nerve conduction is not necessary for the release of these substances in the guinea pig bronchus.
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 (November 1, 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 in the host response to a virus infection.
4

Weinstock, J. V., and A. M. Blum. "Tachykinin production in granulomas of murine schistosomiasis mansoni." Journal of Immunology 142, no. 9 (May 1, 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 collagenase and cultured in vitro for up to 4 h. Only immunoreactive SP appeared in the culture medium. SP immunoreactivity localized solely to granuloma eosinophils as demonstrated by a sensitive immunohistochemical technique. An antiserum that recognized SK, neuropeptide K, and neurokinin B, but which possessed low reactivity to SP, also stained these cells. Only prior absorption of each antiserum with the appropriate synthetic neuropeptide would abrogate the immunostaining. This suggested that tachykinins other than SP were present within these cells. However, results of in situ hybridization experiments intimated that eosinophils produced predominantly preprotachykinin mRNAs which encode SP but are devoid of the SK/neuropeptide K sequence. It is concluded that granuloma eosinophils make predominantly SP in deference to other tachykinins, and that tachykinins other than SP are unlikely to be important in the regulation of the early granulomatous response of murine schistosomiasis.
5

Culman, Juraj, and Thomas Unger. "Central tachykinins: mediators of defence reaction and stress reactions." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 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 hypothalamic NK1 receptors in conscious rats induces an integrated cardiovascular, behavioural, and endocrine response. The cardiovascular response is associated with increased sympathoadrenal activity and comprises an increase in blood pressure and heart rate, mesenteric and renal vasoconstriction, and hind-limb vasodilatation. The behavioural response consists of increased locomotion and grooming behaviour. This response pattern is consistent with an integrated stress response to nociceptive stimuli and pain in rodents. Several studies have demonstrated rapid changes in substance P levels and its receptors in distinct brain areas following acute stress. These data indicate that substance P and other tachykinins, in addition to serving as nociceptive and pain transmitters in the spinal cord, may act in the brain as neurotransmitters–neuromodulators within the neuronal circuits mediating central stress responses.Key words: tachykinins, substance P, central nervous system, defence reaction, stress.
6

Weil, M., A. Itin, and E. Keshet. "A role for mesenchyme-derived tachykinins in tooth and mammary gland morphogenesis." Development 121, no. 8 (August 1, 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 gland; mRNA encoding the neutral endopeptidase (NEP) that degrades secreted tachykinins is spatially and temporally co-expressed with tachykinin precursor mRNA. (3) SP and the mRNA encoding SP receptors are also expressed in the developing tooth germ. (4) Tooth development in explant cultures is blocked both by tachykinin-precursor-specific antisense oligonucleotide and by an SP receptor antagonist: in both cases the block is relieved by exogenous SP. Together, these findings suggest a surprising new role for tachykinins in tooth and mammary gland morphogenesis, and possibly also in limb, ear and external genitalia morphogenesis.
7

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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8

Goto, Tetsuya, and Teruo Tanaka. "Tachykinins and tachykinin receptors in bone." Microscopy Research and Technique 58, no. 2 (July 15, 2002): 91–97. http://dx.doi.org/10.1002/jemt.10123.

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9

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 (March 1, 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 caused an initial hypertension induced by a general vasoconstriction, followed eventually by an elevated flow in both gut arteries due to dilation of the vascular beds. Trout NKA evoked a short-lasting increase in celiac blood flow due to a decrease in vascular resistance, a late decrease in mesenteric flow due to vasoconstriction, and no effect on the somatic vasculature. None of the peptides affected heart rate. The study demonstrates a significant vasoactive function of fish tachykinins in the vascular system of an elasmobranch species and, in addition, the occurrence of tachykinin receptor subtypes. Immunohistochemistry revealed a NKA/SCY II-like peptide in nerve fibers innervating many vessels, including the celiac and the mesenteric arteries, the gastrointestinal canal, and the heart.
10

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 (October 1, 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 sequence of the neurokinin A-related tachykinin at its COOH-terminus. Both trout substance P and neurokinin A stimulated the motility of isolated trout intestinal muscle [pD2(-log of EC50) values 8.5 +/- 0.15 and 7.35 +/- 0.08, respectively] and the vascularly perfused trout stomach (pD2 values 9.63 +/- 0.23 and 8.18 +/- 0.23, respectively). Trout substance P was 14 times more potent than trout neurokinin A in the intestine and 28 times more potent in the stomach. The data suggest that receptors interacting with tachykinins in the trout gastrointestinal tract have a similar selectivity as the mammalian NK-1 receptor.
11

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 (August 1, 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 edema ( P < 0.05) than that observed in paired wild-type mice. Capsaicin (which releases endogenous neuropeptides) and exogenous tachykinins induced edema formation, which was reduced by the mast cell amine histamine H1antagonist mepyramine ( P < 0.05). These findings confirm that tachykinins mediate edema formation via the NK1receptor and provide direct evidence that the septide-sensitive binding site is on the NK1receptor. Furthermore, results suggest that edema induced by the tachykinins, although totally dependent on NK1receptor-mediated mechanism, contains a mast cell-dependent component. The evidence is in keeping with an NK1receptor on mast cells.
12

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 (лютий 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 ligand substance P (SP) resulted in NF-κB activation, as judged by transcription of an NF-κB-luciferase reporter gene and production of interleukin-8, a chemokine whose expression is upregulated by NF-κB. SP caused a dose-dependent activation of NF-κB that was inhibited by the selective Tacr1 antagonist RP67580. Tacr1 is a G protein-coupled receptor capable of activating both the Gq and Gs families of G proteins. Expression of inhibitory peptides and constitutively active G protein mutants revealed that Gq signaling was both necessary for Tacr1-induced NF-κB activation and sufficient for NF-κB activation in the absence of any other treatment. Treatment with pharmacological inhibitors to investigate events downstream of Gq revealed that Tacr1-induced NF-κB activation proceeded through an intracellular signaling pathway that was dependent on phospholipase C, calcium, Ras, Raf-1, MEK, Erk, and proteasome function. These results identify intracellular signaling mechanisms that underlie the proinflammatory effects of tachykinins, which previously have been implicated in lung injury and disease.
13

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 (May 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 animal. In addition, the time to reach the steady-state burst frequency (>2 h) was lengthened in spantide II. These data indicate that an endogenous tachykinin release contributes to the ongoing activity of the locomotor network by modulating the glutamate–glycine neuronal network responsible for the locomotor pattern. We also explored the effects of a 10-min exogenous application of substance P (1 μM), a tachykinin, and showed that its effect on the burst rate depended on the initial NMDA induced burst frequency. At low initial burst rates (∼0.5 Hz), tachykinins caused a marked further slowing to 0.1 Hz, whereas at higher initial burst rates, it instead caused an enhanced burst rate as previously reported, and in addition, a slower modulation (0.1 Hz) of the amplitude of the motor activity. These effects occurred during an initial period of ∼1 h, whereas a modest long-lasting increase of the burst rate remained after >2 h.
14

Leon, Silvia, and Víctor M. Navarro. "Novel Biology of Tachykinins in Gonadotropin-Releasing Hormone Secretion." Seminars in Reproductive Medicine 37, no. 03 (May 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 timing of the preovulatory luteinizing hormone surge in females. Therefore, the action of tachykinins in reproduction appears to extend to all the critical aspects required for the successful attainment and maintenance of fertility. In this review, we summarize the latest advances in our understanding of the biology of tachykinins in the control of GnRH release, addressing the existing controversies, open questions, and future perspectives.
15

Graham, Gwenda J., Joanne M. Stevens, Nigel M. Page, Andrew D. Grant, Susan D. Brain, Philip J. Lowry, and Jonathan M. Gibbins. "Tachykinins regulate the function of platelets." Blood 104, no. 4 (August 15, 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 stimulates platelet aggregation, and underlying this is the intracellular mobilization of calcium and degranulation. We demonstrate the presence of the tachykinin receptors NK1 and NK3 in platelets and present evidence for the involvement of NK1 in SP-mediated platelet aggregation. Platelets were found to contain SP-like immunoreactivity that is secreted upon activation implicating SP-like substances in the autocrine/paracrine regulation of these cells. Indeed, NK1-blocking antibodies inhibited aggregation in response to other agonists. Of particular note is the observation that EKA/B cross-react in the SP immunoassay and are also able to stimulate platelet activation. Together our data implicate tachykinins, specifically SP and EKA/B, in the regulation of platelet function.
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 (June 1, 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 chronotropic response to capsaicin was markedly potentiated in another group of hearts with the further addition of 0.5 μM neostigmine to inhibit cholinesterases. In this group, capsaicin decreased heart rate by 30 ± 10% from a baseline of 214 ± 6 beats/min ( n = 8, P < 0.05). This large bradycardic response to capsaicin was inhibited by 1) infusion of neurokinin A to desensitize tachykinin receptors or 2) treatment with 1 μM atropine to block muscarinic receptors. The latter observations implicate tachykinins and acetylcholine, respectively, as mediators of the bradycardia. These findings support the hypothesis that endogenous tachykinins could mediate axon reflexes to stimulate cholinergic neurons of the intrinsic cardiac ganglia.
17

Patak, Eva, M. Luz Candenas, Jocelyn N. Pennefather, Sebastian Ziccone, Alison Lilley, Julio D. Martín, Carlos Flores, Antonio G. Mantecón, Margot E. Story, and Francisco M. Pinto. "Tachykinins and tachykinin receptors in human uterus." British Journal of Pharmacology 139, no. 3 (June 2003): 523–32. http://dx.doi.org/10.1038/sj.bjp.0705279.

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18

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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19

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 (February 2004): 1445–63. http://dx.doi.org/10.1016/j.lfs.2003.09.039.

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20

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 (November 1, 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 antigen and substance P, but not histamine, were abolished by pretreatment with the tachykinin antagonists [D-Arg1, D-Pro2, D-Trp7,9, Leu11]-substance P and [D-Pro2, D-Trp7,9]-substance P. Interpretation of such results was complicated by the fact that such antagonists may in themselves induce mast cell activation. Depletion of substance P containing neurons by pretreatment of guinea pigs with capsaicin also produced significant inhibition of antigen-induced permeability changes. These results indicate a possible role for tachykinins, such as substance P, in cutaneous anaphylaxis in the guinea pig.
21

Cook, G. A., D. Elliott, A. Metwali, A. M. Blum, M. Sandor, R. Lynch, and J. V. Weinstock. "Molecular evidence that granuloma T lymphocytes in murine schistosomiasis mansoni express an authentic substance P (NK-1) receptor." Journal of Immunology 152, no. 4 (February 15, 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 receptors designated NK-1, NK-2, and NK-3. The NK-1 receptor binds only SP with high affinity. Using reverse transcription-PCR, cDNA cloning, and sequence analysis, we showed that granulomas isolated from the liver of infected mice express an authentic SP (NK-1) receptor but have no detectable neurokinin A (NK-2) and neurokinin B (NK-3) receptor mRNA, as determined by PCR. CD4+ granuloma T lymphocytes, purified by FACS, express NK-1 receptor mRNA. Normal liver devoid of granulomas exhibited none of the three tachykinin receptor subclasses.
22

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 (March 1, 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 contraction-late distention phases were frequently accompanied by phasic contractions with a frequency of 2-4/min. Atropine had a significant effect on the sustained contraction phase but no effect on the phasic contractions or distention phases. Bilateral cervical vagotomy had a significant effect on the early distention phase, suggesting a link with brain stem mechanisms. The activity of brain stem units that responded to phasic distention of the stomach reflected the tachykinin-induced changes in gastric distention. Although the gastric effects of these tachykinins shared distinct similarities, certain differences in the time sequence of the distention-contraction interactions suggests the possibility that dissimilar receptor types may be involved in the mechanisms of action. Their mechanisms of action may also involve a direct effect on the effector organ.
23

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 (December 1, 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 was mimicked by stimulation of the dorsal root, suggesting that dorsal root afferents may be a source of endogenous tachykinin input to the spinal cord. The depolarization was reduced by removal of sodium or calcium from the Ringer, or when potassium conductances were blocked, and was not associated with a measurable change in input resistance. Dorsal root stimulation also caused a depolarization in the dorsal cells, and this effect and that of bath-applied substance P, was blocked by the tachykinin antagonist spantide. 3. The tachykinin substance P could reduce inward and outward rectification in the dorsal cells, the effect on outward rectification only being seen when potassium conductances were blocked by tetraethylammonium (TEA). 4. Substance P increased the excitability of the dorsal cells and giant interneurons, shown by the increased spiking in response to depolarizing current pulses. The increased excitability was blocked by the tachykinin antagonist spantide. 5. Substance P modulated the dorsal cell action potential, by increasing the spike duration and reducing the amplitude of the afterhyperpolarization. The spike amplitude was not consistently affected. 6. Stimulation of the dorsal column resulted in either depolarizing or hyperpolarizing potentials in the giant interneurons. The amplitude of the depolarization was increased by substance P, whereas the amplitude of the hyperpolarization was reduced. These effects occurred independently of a measurable change in postsynaptic input resistance, suggesting that the modulation occurred presynaptically. Paired recordings from dorsal cells and giant interneurons failed to reveal an effect of substance P on dorsal cell-evoked excitatory postsynaptic potentials (EPSPs), suggesting that the potentiation of the dorsal column-evoked depolarization was due to an effect on other axons in the dorsal column. Dorsal root-evoked potentials could also be increased in the presence of substance P, although this effect was less consistent than the effect on dorsal column stimulation. 7. These results suggest that tachykinins modulate sensory input to the lamprey spinal cord by increasing the excitability of primary afferents and second-order giant interneurons, and also by modulating synaptic transmission. Tachykinins may result in potentiation of local spinal reflexes and also modulation of descending reticulospinal inputs to the spinal locomotor network as a result of potentiation of spinobulbar inputs.
24

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 (July 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 are three distinct tachykinin receptors, called NK-1, NK-2 and NK-3. SP binds the NK-1 receptor with highest affinity. Specific NK-1 receptor antagonists blocked all tachykinin-induced, IFN-gamma secretion. An NK-2 receptor inhibitor had no effect. Thus, SP and other tachykinins were acting through an NK-1 receptor. Inflammatory cells from 4-day-old granulomas cultured in vitro secrete IFN-gamma. Yet, there was no measurable IFN-gamma when SP receptor antagonists were added to the cultures. Moreover, animals treated in vivo with the NK-1 receptor antagonist CP-96,345 produced smaller granulomas. This suggested that endogenous SP may be necessary for normal induction of granuloma IFN-gamma secretion and a normal granulomatous response. Granuloma macrophages make somatostatin (SOM) that can decrease IFN-gamma secretion. Yet, IFN-gamma secretion was unaffected when both SP and SOM were in the cell cultures. In conclusion, SP modulates Ag-driven IFN-gamma secretion through a NK-1 receptor. Also, SP and SOM may be components of a natural circuit within inflammation that regulates IFN-gamma production.
25

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 (October 1, 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 of potency of tachykinins in causing contraction, NK greater than SP greater than SK, was similar in both muscle cell types. The results obtained in isolated muscle cells were closely paralleled by results obtained in intact muscle strips; the main difference was the greater sensitivity of isolated cells to tachykinin agonists (250-fold) and antagonist (210-fold). The inhibitory dissociation constant (Ki) of [D-Pro2, D-Trp7,9]substance P estimated from the displacement of dose-response curves (muscle cells) or from Schild plots (muscle strips) differed minimally or not at all, when either SP or SK was used as agonist, consistent with interaction of the two peptides with the same receptor subtype. The notion of a single receptor subtype in ileal muscle cells of the guinea pig was further supported by the occurrence of complete cross-desensitization between SP and SK in muscle strips.
26

Vannucchi, Maria Giuliana, and Stefano Evangelista. "Neurokinin receptors in the gastrointestinal muscle wall: cell distribution and possible roles." BioMolecular Concepts 4, no. 3 (June 1, 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 antibodies has allowed identifying the sites of distribution of the neurokinin receptors in the gut, and important differences have been found among cell types and animal species. The complexity of the receptor distribution, either intraspecies or interspecies, is in agreement with the variegated picture coming out from physiological and pharmacological experiments. Interestingly, most of the knowledge on the tachykinin systems has been obtained from pathological conditions. Here, we tried to collect the main information available on the cellular distribution of the neurokinin receptors in the gut wall in the attempt to correlate their cell location with the several roles the tachykinins seem to play in the gastrointestinal apparatus.
27

Almeida, T. A., J. Rojo, P. M. Nieto, F. M. Pinto, M. Hernandez, J. D. Martín, and M. L. Candenas. "Tachykinins and Tachykinin Receptors: Structure and Activity Relationships." Current Medicinal Chemistry 11, no. 15 (August 1, 2004): 2045–81. http://dx.doi.org/10.2174/0929867043364748.

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28

Von Essen, S. G., S. I. Rennard, D. O'Neill, R. F. Ertl, R. A. Robbins, S. Koyama, and I. Rubinstein. "Bronchial epithelial cells release neutrophil chemotactic activity in response to tachykinins." American Journal of Physiology-Lung Cellular and Molecular Physiology 263, no. 2 (August 1, 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 supernatant fluids induced significant neutrophil chemotaxis compared with supernatants obtained from unstimulated BBEC. Maximal effect was observed after 48 h of incubation and at SP concentration of 10(-13) M [92 +/- 3 (SP) vs. 64 +/- 2 (media) cells/high-power field (HPF), mean +/- SE, n = 7, P less than 0.05]. Release of NCA was mediated by the COOH-terminal of the SP molecule. The rank order of potency of tachykinins in inducing release of NCA was SP greater than NKA = NKB. SP-induced response was significantly potentiated by phosphoramidon (109 +/- 3 vs. 92 +/- 3 cells/HPF, n = 7, P less than 0.05), whereas other proteinase inhibitors had no effect. The released NCA was composed of protein and lipid-soluble components. These data indicate that mammalian tachykinins induce the release of NCA from BBEC and that NEP modulates these effects. We suggest that tachykinins regulate neutrophil recruitment into the lower respiratory tract, in part, by inducing the release of NCA from airway epithelial cells.
29

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 (December 1, 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 gastric mucosal blood flow and was not associated with increased acid secretion. NK2-receptor blockade antagonized the protective effects of [Ala5,beta-Ala8]NKA-(4-10) and NKA-(4-10), whereas NK1-receptor blockade was ineffective. Blockade of NK2 but not NK1 receptors prevented by 65% the protection evoked by topical capsaicin without affecting capsaicin-induced hyperemia. We conclude that the increase in gastric mucosal resistance evoked by tachykinins is NK2 receptor-mediated and involves primary afferent neurons, CGRP, and NO. Gastric mucosal hyperemia and increased acid secretion do not participate in the effect. Tachykinins activating NK2 receptors contribute to the increase in gastric mucosal resistance but not the increment in mucosal blood flow after primary afferent nerve stimulation by capsaicin.
30

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 (July 1, 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. tachykinins elicited dose-dependent increases in MAP and HR (NPK > NPγ > SP > NKA > NKB). The cardiovascular response to i.t. SP, NPK, and NPγ was significantly attenuated by the prior i.t. administration of (±)-CP-96345 and RP-67580 but not by SR-48968 and R-486. By the i.c.v. route, tachykinins also elicited pressor and tachycardiac responses dose dependently (NPK > NPγ > SP > NKA > NKB). Senktide and [MePhe7]NKB, two NK3-selective agonists, were slightly more potent than NKB on both parameters. Whereas the cardiovascular response to NPK was largely blocked by (±)-CP-96345 and RP-67580, that to SP was reduced by 40–50%. This treatment had no effect on the cardiovascular response to NKA and [MePhe7]NKB. Conversely, SR-48968 reduced by 40–50% the NKA-induced cardiovascular changes without affecting the central mediated effects of NPK, SP, and [MePhe7]NKB. However, when coadministered, RP-67580 and SR-48968 abolished the effects to SP and NKA while leaving untouched those induced by [MePhe7]NKB. Finally, the central effects mediated by [MePhe7]NKB, senktide, and NKB were blocked by R-486. These findings suggest that the i.t. action of tachykinins on the rat cardiovascular system is mediated by a NK1 receptor in the spinal cord, while NK1, NK2, and NK3 receptors are likely involved in the supraspinal (hypothalamus) effects of these neuropeptides. It is also concluded that NPK is a pure and powerful NK1 agonist, in contrast to SP and NKA, which are not selective for NK1 or NK2 receptors, respectively.Key words: tachykinins, spinal cord, central cardiovascular control, tachykinin receptor antagonists.
31

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 (June 1, 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 degradation of endogenously released and exogenously administered substance P and neurokinin A, both in normal and asthmatic subjects. As for other indirect bronchoconstrictor stimuli, the effect of neurokinin A on airway calibre in asthmatics can be inhibited by pretreatment with nedocromil sodium. Evidence is accumulating, not only from studies in animals but also from experiments on human airways, that tachykinins may also cause mucus secretion and plasma extravasation. They also have important proinflammatory effects, such as the chemoattraction of eosinophils and neutrophils, the adhesion of neutrophils, and the stimulation of lymphocytes, macrophages and mast cells. The tachykinins interact with the targets on the airways by specific tachykinin receptors. The NK1 and the NK2 receptor have been characterized in human airways, both pharmacologically and by cloning. The NK2 receptor is responsible for the in vitro contraction of normal airways, whilst the NK1 receptor is responsible for most of the other airway effects. Because of their presence in the airways and because of their ability to mimic the various pathophysiological features of asthma, substance P and neurokinin A are presently considered as possible mediators of asthma. The present development of potent and selective tachykinin antagonists will allow us to further define the role of tachykinins in the pathogenesis of asthma.
32

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 (July 1, 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 relevant models of pathophysiological conditions. Tachykinin NK1 and NK2 receptor antagonists reduced the plasma extravasation in the trachea and nasal mucosa and the bronchoconstriction caused by antigen challenge in sensitized guinea-pigs. Blockade of kinin B2 receptors with the selective antagonist HOE-140 had a similar inhibitory effect. The magnitude of the inhibition observed with the kinin receptor antagonist alone was similar to that caused by a combination a tachykinin and kinin receptor antagonists. This suggests activation of a common final pathway by these two groups of mediators. Pharmacological and biochemical evidence suggests that in the airways of sensitized guinea-pigs, kinins released by the anaphylactic reaction stimulate the release of tachykinins from sensory nerves, thus contributing to their proinflammatory action.Key words: kinins, tachykinins, neurogenic inflammation, antigen challenge, airways, nitric oxide.
33

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

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34

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 (1 грудня 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 to that of genuine tachykinins. We conclude that peptides based on Aβ(25–35) but with a Phe residue at position 31 do display properties typical of a tachykinin, but that peptides with Ile at this position do not.
35

Rogers, Duncan F. "Neurokinin receptors subserving airways secretion." Canadian Journal of Physiology and Pharmacology 73, no. 7 (July 1, 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 intestinal peptide (VIP) and neuropeptide tyrosine (NPY), are colocalised and coreleased with the classical neurotransmitter. Investigation of the contribution of the orthodromic neural pathway to neurogenic secretion awaits development of selective receptor antagonists for VIP and NPY. The neurotransmitters of the sensory-efferent neural pathway include calcitonin gene related peptide and the tachykinins substance P and neurokinin A. The order of potency of the natural tachykinins and synthetic selective tachykinin receptor agonists indicates that the tachykinin NK1 receptor is ubiquitous for airway secretory processes, including mucus secretion and ion transport. Antagonist studies show that the great proportion of the NANC neural mucus secretory response is mediated via NK1 receptors, with little or no contribution from NK2 receptors. The relevance of the sensory-efferent neural pathway in health is equivocal, but it may have increasing importance in chronic inflammatory bronchial diseases associated with mucus hypersecretion, for example, asthma and chronic bronchitis, in which there is some evidence for the potential for increased sensory-efferent neural activity.Key words: tachykinin, sensory nerves, mucus, mucus secretion, asthma.
36

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 (May 2005): 2743–51. http://dx.doi.org/10.1111/j.1460-9568.2005.04088.x.

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37

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 (January 2005): 835–62. http://dx.doi.org/10.1016/j.lfs.2004.10.004.

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38

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 (December 1, 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 contrast to IACh, INKA and ISP were not facilitated by increases in internal Ca2+, but little or no current was activated by these peptides when extracellular Ca2+ was low. INKA (10(-7) M) and ISP (10(-5) M) were blocked by Cd2+ (5 x 10(-4) M), quinine (10(-3) M), and the tachykinin-receptor antagonist [D-Pro2,D-Trp7,9]SP (10(-5) M). Current clamp recordings and intracellular recordings of intact tissues showed that NKA and SP depolarized the cell membrane, which is consistent with the activation of a nonselective cation conductance. These data suggest that a primary mechanism of the tachykinins is to activate a nonselective cation conductance that leads to depolarization. The increase in Ca2+ entry due to tachykinin stimulation appears to be secondary to the activation of the nonselective cation conductance.
39

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 (August 1, 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) significantly inhibited both SP-induced depolarization and the stimulation-evoked slow EPSP, as did NK3 receptor desensitization with senktide. Capsaicin, which causes the release of SP from small-diameter afferent fibers, induced a depolarization that was similar to the evoked slow EPSP in both amplitude and duration. The capsaicin-induced depolarization was significantly attenuated in the presence of SR-142801. These data indicate that tachykinins, released from extrinsic afferent fibers, act via NK3 receptors to provide slow excitatory synaptic input to SO neurons.
40

Figini, M., C. Emanueli, E. F. Grady, K. Kirkwood, D. G. Payan, J. Ansel, C. Gerard, P. Geppetti, and N. Bunnett. "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 (April 1, 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 and B2 receptors, respectively. Stimulation of sensory nerves with capsaicin also induced extravasation. Capsaicin- and bradykinin-stimulated extravasation was attenuated by an NK1-receptor antagonist and is thus mediated by release of tachykinins and activation of the NK1 receptor. We conclude that 1) substance P stimulates extravasation in the gastrointestinal tract and pancreas of mice by interacting with the NK1 receptors, and 2) capsaicin and bradykinin induce plasma extravasation by stimulating tachykinin release from sensory nerves. Thus neurogenic mechanisms mediate inflammation in the gastrointestinal tract and pancreas of the mouse.
41

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 (September 1, 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 the CAP-O3 group compared with the O3-exposed group. In better agreement with our initial hypothesis, the CAP-O3 group was less responsive than the O3-exposed animals to histamine aerosol challenge. Additionally, Evans blue dye accumulation, a hallmark of tachykinin release, was increased in O3-exposed animals and was partially blocked in the CAP-O3 group. These data suggest that tachykinin-containing sensory fibers are unlikely to mediate the acute effects of O3 exposure on tidal breathing and lavage fluid protein accumulation but may play a role in causing post-O3 airway hyperreactivity and protein extravasation into the trachea.
42

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 (December 1, 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. To test these hypotheses, we analyzed respiratory system resistance changes and Evans blue-labeled albumin extravasation into the airways of 60 tracheostomized and mechanically ventilated guinea pigs. Animals were subjected to 10 min of isocapnic dry gas hyperpnea or to quiet breathing of humidified gas and received as pretreatment either piroxicam, a cyclooxygenase (CO) inhibitor; A-63162, a 5-lipoxygenase (5-LO) inhibitor; BW-755c, a combined CO and 5-LO inhibitor; ICI-198,615, a leukotriene D4 receptor antagonist; or no drug. HIB was substantially (50–80%) reduced by each of the four eicosanoid-modulating drugs. In contrast, HIBVH was reduced only by BW-755c, and this effect occurred only within the extrapulmonary airways (42% reduction). These data indicate that both CO and 5-LO products, including leukotriene D4, participate in the pathogenesis of HIB but that, like tachykinins, they play only a small contributory role in HIBVH. Together with our previous demonstration that sensory neuropeptide release is critical for the occurrence of HIB, we conclude that the roles of eicosanoids and tachykinins in guinea pig HIB are interdependent.
43

Grundy, Luke, Russ Chess-Williams, Stuart M. Brierley, Kylie Mills, Kate H. Moore, Kylie Mansfield, Roselyn Rose’Meyer, Donna Sellers, and David Grundy. "NKA enhances bladder-afferent mechanosensitivity via urothelial and detrusor activation." American Journal of Physiology-Renal Physiology 315, no. 4 (October 1, 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 neurons. Bath application of NKA induced concentration-dependent increases in bladder-afferent firing and intravesical pressure that were attenuated by nifedipine and by the NK2 receptor antagonist GR159897 (100 nM). Intravesical NKA significantly decreased bladder compliance but had no direct effect on mechanosensitivity to bladder distension (30 µl/min). GR159897 alone enhanced bladder compliance but had no effect on mechanosensation. Intravesical NKA enhanced both the amplitude and frequency of bladder micromotions during distension, which induced significant transient increases in afferent firing, and were abolished by GR159897. NKA increased intracellular calcium levels in primary urothelial cells but not bladder-innervating DRG neurons. Urothelial ATP release during bladder distention was unchanged in the presence of NKA, whereas acetylcholine levels were reduced. NKA-mediated activation of urothelial cells and enhancement of bladder micromotions are novel mechanisms for NK2 receptor-mediated modulation of bladder mechanosensation. These results suggest that NKA influences bladder afferent activity indirectly via changes in detrusor contraction and urothelial mediator release. Direct actions on sensory nerves are unlikely to contribute to the effects of NKA.
44

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

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45

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

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46

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 (April 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 tachykinins reacts with material in the posterior part of the central lobe of paraformaldehyde-fixed salivary glands. The presence of a vasodilatory peptide of the tachykinin family in the salivary glands of A. aegypti is proposed and its role in blood feeding is discussed.
47

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 (July 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 aerosols from 2(-5)% (wt/vol) until the transpulmonary pressure increased more than twofold from the baseline. After the final exposure, we exposed them to phosphoramidon (10(-4) M) or its vehicle. Phosphoramidon significantly potentiated the increased RL induced by OVA challenge. Phosphoramidon also significantly potentiated the increased RL in the guinea pigs treated with atropine, but the potentiation was significantly reduced. In contrast, phosphoramidon failed to potentiate the increased RL induced by OVA in guinea pigs pretreated with capsaicin. These results suggest that 1) endogenous tachykinin-like substances are released in allergic airway response and that 2) when endogenous NEP is inhibited in the guinea pig airways in vivo, the substances contribute to bronchoconstriction by partly activating the parasympathetic nerve.
48

Kinberg, Kirk, and Roger H. Kobayashi. "ACROLEIN INCREASES AIRWAY SENSITIVITY TO SUBSTANCE P AND DECREASES NEP ACTIVITY IN GUINEA PIGS." Pediatrics 94, no. 2 (August 1, 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) which are found in airway epithelium and smooth muscle. Airway damage may cause enhanced tachykinin-induced effect. The purpose of this study was to investigate the inter-relationship between tachykinins and reduced NEP on the effects of pulmonary functions as well as bronchoalveolar lavage findings. Methods. Guinea pigs were given an aerosolized solution of acrolein, a component of cigarette smoke and smog, which is known to cause epithelial cytotoxicity and increased sensitivity to acetylcholine. Pulmonary functions were measured via body box. Dose response curves were calculated from subject guinea pigs given the acrolein as well as the control group following substance P administration. Subsequently, subject as well as control guinea pigs were exposed to thiorphan to inhibit NEP. They were then given subsequent challenges of either IV or aerosolized substance P and pulmonary testing as well as bronchoalveolar lavage was performed. NEP activity was measured at 1, 7, and 28 days after exposure. Results. Pulmonary intonation and epithelial damage were prominent on the day after acrolein exposure showing influx of monocytes, neutrophils, and epithelial damage.
49

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 (September 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 therefore explores whether tachykinins also use the endocannabinoid system to modulate the locomotor frequency. By monitoring fictive locomotion, we were able to compare the facilitatory effects exerted by applying substance P (1 μM, 20 min), on the burst frequency before and during application of the endocannabinoid CB1 receptor antagonist AM251 (2–5 μM). By using two different lamprey species, we showed that the response to substance P on the burst frequency is significantly reduced during the application of AM251. To examine whether endocannabinoids are involved in the substance P–mediated modulation of reciprocal inhibition, the commissural axons were stimulated, while recording intracellularly from motoneurons. We compare the effect of substance P on the amplitude of the contralateral compound glycinergic inhibitory postsynaptic potential (IPSP) in control and in the presence of AM251. The blockade of CB1 receptors reduced the substance P–mediated decrease in the amplitude by 29%. The present findings suggest that the effects of substance P on the increase in the locomotor burst frequency and depression of IPSPs are mediated partially via release of endocannabinoids acting through CB1 receptors.
50

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 (September 1, 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 169 +/- 6.1% of control. In contrast, NKA and NKB had little and no effect on ASM cell growth, respectively. Because SP is nonselective in its binding to the tachykinin receptors, to identify the specific NK receptor subtype(s) mediating the promitogenic action of SP, in separate studies we found that 1) the NK1-receptor-specific agonist, [beta-Ala4, Sar9, Met(O2)11]SP-(4-11) induced stimulation of ASM cell growth similar in magnitude to that elicited by SP; 2) in contrast, neither the NK1- nor NK2-receptor-specific agonists, [beta-Ala8]NKA-(4-10) and [MePhe7]NKB, respectively, had any effect on ASM cell growth; and 3) the promitogenic action of SP was inhibited by the NK1-receptor antagonist, GR-82,334. Moreover, in extended experiments, we found that the phospholipase C and phospholipase A2 inhibitors, neomycin and quinacrine, respectively, each inhibited SP-induced ASM cell proliferation by approximately 45%. Collectively, these observations provide new evidence that the tachykinin SP induces ASM cell proliferation, and that this action is mediated by transmembrane signaling coupled to selective activation of the NK1 receptor.

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