Lüscher T F
Departement Innere Medizin, Kantonsspital Basel.
Schweiz Rundsch Med Prax. 1993 Oct 19;82(42):1148-53.
While nitrates have been in clinical use for more than 100 years, their mode of action is of rather recent discovery. Nitrates act by the release of the free radical NO (nitric oxide) which stimulates the cyclic guanosine monophosphate as vasodilatator and as inhibitor of platelet function. The endogenous nitrate NO is derived from L-arginine catalyzed by nitric oxide synthase, a recently cloned enzyme. Nitrates and other nitro-vasodilatators act similarly to the endogenous nitrate, whereby a basal release of NO in the vascular wall reduces the effect of nitro-vasodilatators. Therefore, drugs are particularly effective in endothelium-free vessel segments and in veins, where the basal release of NO is low. A recently discovered effect of nitro-vasodilatators is the inhibition of thrombin and angiotensin II-induced production of endothelin. Insofar the L-arginine/NO metabolism acts as an important regulator in the vessel wall and has a protective role in the circulation by its antispastic and antithrombotic principle.
虽然硝酸盐已在临床应用超过100年，但其作用方式是最近才发现的。硝酸盐通过释放自由基NO（一氧化氮）起作用，NO刺激环磷酸鸟苷作为血管扩张剂并作为血小板功能的抑制剂。内源性硝酸盐NO源自一氧化氮合酶催化的L-精氨酸，一氧化氮合酶是一种最近克隆的酶。硝酸盐和其他硝基血管扩张剂的作用类似于内源性硝酸盐，血管壁中NO的基础释放会降低硝基血管扩张剂的作用。因此，药物在无内皮血管段和静脉中特别有效，因为那里NO的基础释放较低。硝基血管扩张剂最近发现的作用是抑制凝血酶和血管紧张素II诱导的内皮素产生。就L-精氨酸/NO代谢而言，它在血管壁中起重要调节作用，并通过其抗痉挛和抗血栓形成原理在循环中起保护作用。
