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速激肽诱导的大鼠鼻液分泌和血浆渗出:肽酶抑制的作用

Tachykinin-induced nasal fluid secretion and plasma exudation in the rat: effects of peptidase inhibition.

作者信息

Lindell E, Svensjö M E, Malm L, Petersson G

机构信息

Department of Otorhinolaryngology, General Hospital, Malmö, Sweden.

出版信息

Neuropeptides. 1995 May;28(5):309-15. doi: 10.1016/0143-4179(95)90047-0.

Abstract

Substance P (SP) evokes fluid secretion and plasma extravasation when applied to the nasal mucosa of rats. SP and another tachykinin, neurokinin A (NKA), are degraded in vitro by neutral endopeptidase (NEP) and angiotensin-1-converting enzyme (ACE). In this study, NKA or SP were applied locally to the nasal mucosa of rats. Subsequent fluid secretion was measured by a filter paper technique. Plasma exudation was derived as the recovery of intravenous (i.v.) administered 125I-albumin from the fluid-containing filter papers. In order to inhibit enzymatic degradation of the tachykinins by NEP and ACE, the rats were treated with i.v. administered phosphoramidon or captopril respectively or their combination. SP evoked fluid secretion that was augmented by phosphoramidon and further enhanced by adding captopril. NKA evoked nasal fluid secretion less effectively than SP and the effect was unaffected by peptidase inhibition. SP, but not NKA, evoked increased plasma exudation but only after pre-treatment with phosphoramidon.

摘要

P物质(SP)作用于大鼠鼻黏膜时可引起液体分泌和血浆外渗。SP和另一种速激肽神经激肽A(NKA)在体外可被中性内肽酶(NEP)和血管紧张素转换酶(ACE)降解。在本研究中,将NKA或SP局部应用于大鼠鼻黏膜。随后通过滤纸技术测量液体分泌。血浆渗出通过从含液体的滤纸中回收静脉注射(i.v.)的125I-白蛋白来计算。为了抑制NEP和ACE对速激肽的酶促降解,分别给大鼠静脉注射磷酰胺或卡托普利或两者联合使用。SP引起的液体分泌可被磷酰胺增强,加入卡托普利后进一步增强。NKA引起鼻液分泌的效果不如SP,且该作用不受肽酶抑制的影响。SP可引起血浆渗出增加,但仅在磷酰胺预处理后出现,而NKA则无此作用。

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