Waeber B, Nussberger J, Brunner H R, de Agostini A, Schapira M
Schweiz Med Wochenschr. 1984 Dec 1;114(48):1749-51.
The active fragment derived from factor XII (factor XIIf) was purified from human plasma and administered intravenously to normotensive conscious rats. Factor XIIf-mediated hypotension was dose-dependent and augmented by pretreatment with captopril, an inhibitor of the angiotensin I- and bradykinin-processing enzyme. In contrast, factor XIIf-induced hypotension was not enhanced by blockade of the renin-angiotensin system by saralasin, a competitive antagonist of angiotensin II at the vascular receptor level. These results suggest that factor XIIf-mediated hypotension is due to the formation of bradykinin.
从人血浆中纯化出源自因子 XII 的活性片段(因子 XIIf),并将其静脉注射给血压正常的清醒大鼠。因子 XIIf 介导的低血压呈剂量依赖性,且可被血管紧张素 I 和缓激肽加工酶抑制剂卡托普利预处理增强。相比之下,在血管受体水平上,血管紧张素 II 的竞争性拮抗剂沙拉新对肾素 - 血管紧张素系统的阻断并未增强因子 XIIf 诱导的低血压。这些结果表明,因子 XIIf 介导的低血压是由于缓激肽的形成。