N-methylnicotinamide inhibits arterial thrombosis in hypertensive rats

被引:1
|
作者
Mogielnicki, A. [1 ]
Kramkowski, K. [1 ]
Pietrzak, L. [1 ]
Buczko, W. [1 ]
机构
[1] Med Univ, Dept Pharmacodynam, PL-15089 Bialystok, Poland
来源
关键词
nicotinamide metabolite; arterial thrombosis; platelets; fibrinolysis; prostacyclin;
D O I
暂无
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
There are few findings indicating that nicotinamide may potentially influence intravascular thrombosis. Interestingly, N-methylnicotinamide, one of the metabolites of nicotinamide - could be more potent than its parent compound. In the present study we have investigated the influence of N-methylnicotinamide on arterial thrombosis in normotensive and renovascular hypertensive rats. The contribution of platelets, coagulation and fibrinolytic systems in the mode of N-methylnicotinamide action was also determined, Furthermore, we examined the role of nitric oxide/prostacyclin in the mechanisms of N-methylnicotinamide action. N-methylnicotinamide, but not nicotinamide, administered intravenously into renovascular hypertensive rats developing electrically induced arterial thrombosis caused dose-dependent decrease of thrombus weight, collagen-induced platelet aggregation and plasma antigen/activity of plasminogen activator inhibitor - 1, without changing of occlusion time, routine coagulation parameters and plasma activity of tissue plasminogen activator. Indomethacin - an inhibitor of prostacyclin synthesis, completely abolished the antithrombotic and antiplatelet effect of N-methylnicotinamide, and the plasma level of 6-keto-PGF(1 alpha), prostacyclin metabolite, increased simultaneously with the inhibition of thrombus formation. Our study shows that N-methylnicotinamide via production/release of prostacyclin inhibits arterial thrombosis development. The antithrombotic effect of N-methylnicotinamide is accompanied by platelet inhibition and enhanced fibrinolysis, due to the decrease production of plasminogen activator inhibitor - 1.
引用
收藏
页码:515 / 527
页数:13
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