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缓激肽诱导豚鼠心房中辣椒素敏感神经释放降钙素基因相关肽:作用机制及钙需求

Bradykinin-induced release of calcitonin gene-related peptide from capsaicin-sensitive nerves in guinea-pig atria: mechanism of action and calcium requirements.

作者信息

Geppetti P, Tramontana M, Santicioli P, Del Bianco E, Giuliani S, Maggi C A

机构信息

Institute of Internal Medicine IV, University of Florence, Italy.

出版信息

Neuroscience. 1990;38(3):687-92. doi: 10.1016/0306-4522(90)90062-9.

DOI:10.1016/0306-4522(90)90062-9
PMID:2270140
Abstract

The mechanism of neuropeptide secretion induced by bradykinin from capsaicin-sensitive afferents was studied in guinea-pig atria. Both the inotropic response induced by bradykinin (0.1 microM) in the electrically driven isolated guinea-pig left atria and the bradykinin (10 microM)-induced release of calcitonin gene-related peptide calcitonin gene-related peptide-like immunoreactivity from slices of guinea-pig atria were abolished in vitro by capsaicin pretreatment or in the presence of indomethacin. Bradykinin-induced calcitonin gene-related peptide-like immunoreactive release was unaffected by tetrodotoxin (0.3 microM), the protein kinase C inhibitor, 1-(5-isoquinolinesulphonyl)-2-methylpiperazine (30 microM), nefedipine (1 microM) or Ruthenium Red (10 microM). It was significantly reduced by 79% in a Ca2(+)-free medium and by 52% in the presence of 0.1 microM omega-conotoxin (fraction GVIA). It is proposed that bradykinin releases calcitonin gene-related peptide from capsaicin-sensitive afferents in guinea-pig atria, via prostanoid generation. This mode of activation of the "efferent" function of capsaicin-sensitive nerves appears to be distinct from those produced by capsaicin or electrical field stimulation as they have been characterized in previous works. In fact, the bradykinin activation of capsaicin-sensitive afferents is not affected by tetrodotoxin and Ruthenium Red, but is partially sensitive to the selective blocker of N-type Ca2(+)-channels, omega-conotoxin.

摘要

在豚鼠心房中研究了缓激肽从辣椒素敏感传入神经诱导神经肽分泌的机制。在体外,辣椒素预处理或吲哚美辛存在时,缓激肽(0.1微摩尔)在电驱动的离体豚鼠左心房中诱导的变力反应以及缓激肽(10微摩尔)诱导的豚鼠心房切片中降钙素基因相关肽样免疫反应性的释放均被消除。缓激肽诱导的降钙素基因相关肽样免疫反应性释放不受河豚毒素(0.3微摩尔)、蛋白激酶C抑制剂1 -(5 -异喹啉磺酰基)- 2 -甲基哌嗪(30微摩尔)、硝苯地平(1微摩尔)或钌红(10微摩尔)的影响。在无钙培养基中显著降低79%,在存在0.1微摩尔ω-芋螺毒素(GVIA组分)时降低52%。提出缓激肽通过前列腺素生成从豚鼠心房中的辣椒素敏感传入神经释放降钙素基因相关肽。辣椒素敏感神经“传出”功能的这种激活模式似乎与辣椒素或电场刺激产生的模式不同,因为它们在先前的研究中已有特征描述。事实上,缓激肽对辣椒素敏感传入神经的激活不受河豚毒素和钌红的影响,但对N型钙通道的选择性阻滞剂ω-芋螺毒素部分敏感。

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