Yoshizumi M, Tsuji H, Nishimura H, Masuda H, Kunieda Y, Kawano H, Kimura S, Sugano T, Kitamura H, Nakagawa K, Nakagawa M
Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
Thromb Haemost. 1999 Nov;82(5):1497-503.
In the present study, we demonstrate that brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP) interact with angiotensin II (Ang II) in regulative blood coagulation and fibrinolysis by suppressing the expressions of both tissue factor (TF) and plasminogen activator inhibitor-1 (PAI-1) induced by Ang II. The expressions of TF and PAI-1 mRNA were analyzed by northern blotting methods, and the activities of TF on the surface of rat aortic endothelial cells (RAECs) and PAI-1 in the culture media were respectively measured by chromogenic assay. Both BNP and CNP suppressed the expressions of TF and PAI-1 mRNA induced by Ang II in a time- and concentration-dependent manner via cGMP cascade, which suppressions were accompanied by respective decrease in activities of TF and PAI-1. However, neither the expression of tissue factor pathway inhibitor (TFPI) nor tissue-type plasminogen activator (TPA) mRNA was affected by the treatment of BNP and CNP.
在本研究中,我们证明脑钠肽(BNP)和C型钠肽(CNP)通过抑制血管紧张素II(Ang II)诱导的组织因子(TF)和纤溶酶原激活物抑制剂-1(PAI-1)的表达,在调节血液凝固和纤维蛋白溶解过程中与Ang II相互作用。采用Northern印迹法分析TF和PAI-1 mRNA的表达,通过显色法分别测定大鼠主动脉内皮细胞(RAECs)表面TF的活性和培养基中PAI-1的活性。BNP和CNP均通过cGMP级联反应以时间和浓度依赖性方式抑制Ang II诱导的TF和PAI-1 mRNA的表达,这种抑制伴随着TF和PAI-1活性的相应降低。然而,BNP和CNP处理对组织因子途径抑制剂(TFPI)的表达以及组织型纤溶酶原激活物(TPA)mRNA均无影响。