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.
Abstract
- 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
- 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。
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