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1
NK2 receptors mediate plasma extravasation in guinea-pig lower airways.NK2受体介导豚鼠下呼吸道的血浆外渗。
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2
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Identification of both NK1 and NK2 receptors in guinea-pig airways.豚鼠气道中NK1和NK2受体的鉴定。
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5
In vivo pharmacology of [beta Ala8]neurokinin A-(4-10), a selective NK-2 tachykinin receptor agonist.
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6
Comparison of tachykinin NK1 and NK2 receptors in the circular muscle of the guinea-pig ileum and proximal colon.豚鼠回肠和近端结肠环形肌中速激肽NK1和NK2受体的比较。
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Effects on the isolated human bronchus of SR 48968, a potent and selective nonpeptide antagonist of the neurokinin A (NK2) receptors.神经激肽A（NK2）受体的强效选择性非肽拮抗剂SR 48968对离体人支气管的作用。
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Involvement of NK1 and NK2 receptors in pulmonary responses elicited by non-adrenergic, non-cholinergic vagal stimulation in guinea-pigs.NK1和NK2受体在豚鼠非肾上腺素能、非胆碱能迷走神经刺激引发的肺部反应中的作用。
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Role of tachykinin NK2-receptor activation in the allergen-induced late asthmatic reaction, airway hyperreactivity and airway inflammatory cell influx in conscious, unrestrained guinea-pigs.速激肽NK2受体激活在变应原诱导的清醒、无束缚豚鼠迟发性哮喘反应、气道高反应性及气道炎性细胞浸润中的作用
Br J Pharmacol. 1999 Jun;127(4):1030-8. doi: 10.1038/sj.bjp.0702628.
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Neurogenic plasma leakage in mouse airways.小鼠气道中的神经源性血浆渗漏。
Br J Pharmacol. 1999 Jan;126(2):522-8. doi: 10.1038/sj.bjp.0702323.
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Involvement of tachykinin receptors in oedema formation and plasma extravasation induced by substance P, neurokinin A, and neurokinin B in mouse ear.速激肽受体在P物质、神经激肽A和神经激肽B诱导的小鼠耳部水肿形成和血浆外渗中的作用。
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Differential effects of phosphoramidon and captopril on NK1 receptor-mediated plasma extravasation in the rat trachea.磷酰胺脒基和卡托普利对大鼠气管中NK1受体介导的血浆外渗的不同作用。
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Identification of both NK1 and NK2 receptors in guinea-pig airways.豚鼠气道中NK1和NK2受体的鉴定。
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7
Involvement of tachykinins in plasma extravasation induced by bradykinin and low pH medium in the guinea-pig conjunctiva.速激肽在豚鼠结膜中由缓激肽和低pH介质诱导的血浆外渗中的作用。
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Vascular protein linkage in various tissue induced by substance P, capsaicin, bradykinin, serotonin, histamine and by antigen challenge.P物质、辣椒素、缓激肽、血清素、组胺以及抗原激发在多种组织中诱导的血管蛋白连接。
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New selective agonists for neurokinin receptors: pharmacological tools for receptor characterization.神经激肽受体的新型选择性激动剂：用于受体表征的药理学工具。
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Histamine release and local responses of rat and human skin to substance P and other mammalian tachykinins.组胺释放以及大鼠和人类皮肤对P物质和其他哺乳动物速激肽的局部反应。
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The role of increased airway microvascular permeability and plasma exudation in asthma.气道微血管通透性增加和血浆渗出在哮喘中的作用。
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Competitive antagonists discriminate between NK2 tachykinin receptor subtypes.竞争性拮抗剂可区分NK2速激肽受体亚型。
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G protein activation: a receptor-independent mode of action for cationic amphiphilic neuropeptides and venom peptides.
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NK2受体介导豚鼠下呼吸道的血浆外渗。

NK2 receptors mediate plasma extravasation in guinea-pig lower airways.

作者信息

Tousignant C, Chan C C, Guevremont D, Brideau C, Hale J J, MacCoss M, Rodger I W

机构信息

Department of Pharmacology, Merck Frosst Centre for Therapeutic Research, Pointe Claire-Dorval, Québec, Canada.

出版信息

Br J Pharmacol. 1993 Feb;108(2):383-6. doi: 10.1111/j.1476-5381.1993.tb12813.x.

DOI:10.1111/j.1476-5381.1993.tb12813.x
PMID:8383563
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1907971/
Abstract
  1. Neurokinin (NK) receptor-mediated extravasation has been examined in guinea-pig airways by use of a recently described marker for microvascular protein leakage, 125I-labelled human fibrinogen. 2. Neurokinin A (NKA) caused a dose-dependent increase in plasma [125I]-fibrinogen extravasation in trachea, main bronchi, secondary bronchi and intraparenchymal airways. In contrast, the NK2 selective agonist [beta-Ala8]NKA(4-10) only caused extravasation in the secondary and intraparenchymal airways. 3. The NK2 selective antagonist, SR 48968, caused a dose-dependent inhibition of NKA and [beta-Ala8]NKA(4-10)-induced extravasation of fibrinogen in guinea-pig secondary bronchi and intraparenchymal airways. SR 48968 was without effect on the NKA-induced extravasation in trachea and main bronchi. 4. NKA- or [beta-Ala8]NKA(4-10)-induced plasma extravasation was not modified by pretreatment with histamine H1- or H2-receptor antagonists. 5. It is concluded that NK2 receptors mediate plasma [125I]-fibrinogen extravasation in guinea-pig secondary bronchi and intraparenchymal airways. This effect is direct and does not depend upon histamine released from mast cells.
摘要
  1. 利用最近描述的微血管蛋白渗漏标志物125I标记的人纤维蛋白原，在豚鼠气道中研究了神经激肽（NK）受体介导的血管外渗。2. 神经激肽A（NKA）导致气管、主支气管、二级支气管和肺实质内气道中血浆[125I] - 纤维蛋白原血管外渗呈剂量依赖性增加。相比之下，NK2选择性激动剂[β - Ala8]NKA(4 - 10)仅在二级支气管和肺实质内气道中引起血管外渗。3. NK2选择性拮抗剂SR 48968在豚鼠二级支气管和肺实质内气道中对NKA和[β - Ala8]NKA(4 - 10)诱导的纤维蛋白原血管外渗产生剂量依赖性抑制。SR 48968对气管和主支气管中NKA诱导的血管外渗没有影响。4. 用组胺H1或H2受体拮抗剂预处理不会改变NKA或[β - Ala8]NKA(4 - 10)诱导的血浆外渗。5. 得出结论，NK2受体介导豚鼠二级支气管和肺实质内气道中血浆[125I] - 纤维蛋白原的血管外渗。这种作用是直接的，不依赖于肥大细胞释放的组胺。