Production of nitric oxide from endothelial cells by 31-amino-acid-length endothelin-1, a novel vasoconstrictive product by human chymase

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• 作者：Niwa ; Yasuharu ; Nagata ; Noriko ; Oka ; Makiko ; Toyoshima ; Toshihiro ; Akiyoshi ; Hiroko ; Wada ; Tomoko ; et. al.
• 关键词：Endothelin ; Endothelium ; Nitric oxide ; Chymase
• 刊名：Life Sciences
• 出版年：2000
• 期刊代码：62_00243205
• 类别：imm
• 出版时间：July 21, 2000
• 卷：67
• 期：9
• 页码：1103-1109
• 文件大小：199 K

摘要

Human chymase selectively converts big endothelin (ET)-1 to 31-amino-acid-length ET-1 [ET-1(1-31)]. In this study we examined effect of ET-1(1-31) on endothelial function. ET-1(1-31) evoked contraction in a concentration-dependent manner at >10⁻⁸ M, which was about 10 times weaker than that of conventional ET-1 [ET-1(1-21)]. BQ485, an ETA receptor antagonist, completely abolished ET-1(1-31)–induced contraction, but BQ788, an ETB receptor antagonist, slightly enhanced it, suggesting that ET-1(1-31) relaxes artery via endothelium. On endothelial cells, ET-1(1-21) and ET-1(1-31) increased [Ca²+]i and produced NO, both of which were significantly inhibited by BQ788 and not by BQ485. These results indicate that ET-1(1-31) increased [Ca²+]i and produced NO in endothelial cells through ETB receptor similarly with ET-1(1-21), although slight diference in effect on smooth muscle cells.