垂体腺苷酸环化酶激活肽诱导豚鼠气道中由环鸟苷酸介导的舒张。

Pituitary adenylate cyclase activating peptide induces cGMP-mediated relaxation in guinea-pig airways.

作者信息

Saotome M, Uchida Y, Nomura A, Endo T, Hasegawa S

机构信息

Department of Pulmonary Medicine, University of Tsukuba, Japan.

出版信息

Pulm Pharmacol Ther. 1998;11(4):281-5. doi: 10.1006/pupt.1998.0120.

DOI:10.1006/pupt.1998.0120

PMID:10101745

Abstract

The mechanism of relaxation of the guinea-pig trachea induced by pituitary adenylate cyclase activating peptide (PACAP)-27 was investigated. We examined whether modulators of nitric oxide (NO) and carbon monoxide (CO) affect PACAP-induced response of tracheal strips in vitro. Pretreatment with N omega-nitro-L-arginine methyl ester hydrochloride (L-NAME) and L-arginine (L-arg) had no effect, while 1H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), haemoglobin and zinc protoporphyrin IX (ZnPP-9) partially abolished the PACAP-induced relaxation. PACAP-27 elevated cyclic GMP level in airway smooth muscle tissue. These results indicate that PACAP-27 not only induces cyclic AMP-mediated responses, but also cyclic GMP-mediated responses in the airway. In addition, CO is related to the PACAP-induced elevation of cGMP level in the tracheal tissue.

摘要

研究了垂体腺苷酸环化酶激活肽（PACAP）-27诱导豚鼠气管舒张的机制。我们检测了一氧化氮（NO）和一氧化碳（CO）的调节剂是否影响体外气管条对PACAP的反应。用盐酸Nω-硝基-L-精氨酸甲酯（L-NAME）和L-精氨酸（L-arg）预处理没有效果，而1H-[1,2,4]恶二唑并[4,3-a]喹喔啉-1-酮（ODQ）、血红蛋白和锌原卟啉IX（ZnPP-9）部分消除了PACAP诱导的舒张。PACAP-27提高了气道平滑肌组织中的环鸟苷酸（cGMP）水平。这些结果表明，PACAP-27不仅诱导气道中环磷酸腺苷（cAMP）介导的反应，还诱导环鸟苷酸介导的反应。此外，CO与PACAP诱导的气管组织中cGMP水平升高有关。