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长须罗蛉的唾液腺匀浆及其血管舒张肽马克西迪兰通过激活PAC1受体导致血浆渗漏。

Salivary gland homogenates of Lutzomyia longipalpis and its vasodilatory peptide maxadilan cause plasma leakage via PAC1 receptor activation.

作者信息

Svensjö Erik, Saraiva Elvira M, Bozza Marcelo T, Oliveira Sandra M P, Lerner Ethan A, Scharfstein Julio

机构信息

Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brasil.

出版信息

J Vasc Res. 2009;46(5):435-46. doi: 10.1159/000197866. Epub 2009 Jan 29.

DOI:10.1159/000197866
PMID:19176972
Abstract

OBJECTIVES

Experiments were designed to determine if salivary gland homogenates (SGH) of the sand fly Lutzomyia longipalpis, the vasodilatory peptides maxadilan and pituitary adenylate cyclase-activating peptide (PACAP-38) may cause plasma leakage and to what extent these effects could be due to PAC1 receptor stimulation.

METHODS

Using FITC-dextran as a plasma marker, intravital microscopy of the hamster cheek pouch (HCP) and a digital camera were used to assess arteriolar diameter and fluorescence of a selected area (5 mm(2)) representative of the HCP microcirculation.

RESULTS

Cheek pouches prepared for intravital microscopy and exposed to topical application of SGH, maxadilan or PACAP-38 developed maximal dilation of arterioles in the range of 20-60 mum within 10 min, and this effect lasted for 30-90 min. The increase in fluorescence intensity induced by each of these compounds was due to plasma leakage from postcapillary venules. The mutant peptide of maxadilan (M-65), a PAC1 receptor antagonist, inhibited both dilation and plasma leakage induced by SGH or maxadilan. Plasma leakage induced by SGH was modestly inhibited by the bradykinin B(2) receptor antagonist HOE-140, but not by the antihistamine mepyramine or the nitric oxide synthase inhibitor L-NA.

CONCLUSIONS

SGH of L. longipalpis and its vasodilatory peptide maxadilan caused long-lasting arteriolar dilation and plasma leakage in the cheek pouch via PAC1 receptor activation.

摘要

目的

设计实验以确定白蛉长须罗蛉的唾液腺匀浆(SGH)、血管舒张肽马克西迪兰和垂体腺苷酸环化酶激活肽(PACAP - 38)是否会导致血浆渗漏,以及这些效应在多大程度上可能归因于PAC1受体的刺激。

方法

使用异硫氰酸荧光素 - 葡聚糖作为血浆标志物,采用仓鼠颊囊(HCP)活体显微镜和数码相机评估代表HCP微循环的选定区域(5平方毫米)的小动脉直径和荧光。

结果

为活体显微镜检查准备的颊囊,局部应用SGH、马克西迪兰或PACAP - 38后,在10分钟内小动脉出现最大程度的扩张,范围在20 - 60微米,且这种效应持续30 - 90分钟。这些化合物各自诱导的荧光强度增加是由于毛细血管后微静脉的血浆渗漏所致。马克西迪兰的突变肽(M - 65),一种PAC1受体拮抗剂,抑制了SGH或马克西迪兰诱导的扩张和血浆渗漏。缓激肽B2受体拮抗剂HOE - 140适度抑制了SGH诱导的血浆渗漏,但组胺拮抗剂美吡拉敏或一氧化氮合酶抑制剂L - NA则没有。

结论

长须罗蛉的SGH及其血管舒张肽马克西迪兰通过激活PAC1受体在颊囊中引起持久的小动脉扩张和血浆渗漏。

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