Saijonmaa O, Ristimäki A, Fyhrquist F
Unit of Clinical Physiology, Minerva Institute for Medical Research, Helsinki, Finland.
Biochem Biophys Res Commun. 1990 Dec 14;173(2):514-20. doi: 10.1016/s0006-291x(05)80064-6.
Atrial natriuretic peptide (ANP) and the nitrovasodilator drugs nitroglycerine and nitroprusside were shown here to decrease both basal and thrombin stimulated production of endothelin-1 (ET-1) from cultured human endothelial cells as measured by radioimmunoassay. 8-Bromo-3',5'-cyclic guanosine monophosphate (cGMP) and papaverine also inhibited ET-1 production. The inhibitory effect of ANP and nitrovasodilators on ET-1 production thus appears to be mediated by guanylate cyclase and cGMP. Part of the vasodilatory action of ANP, nitroprusside and nitroglycerine may be due to suppression of endothelial ET-1 production. This may be an additional mechanism whereby nitrovasodilators participate in the regulation of vascular tone.
本文显示，心房利钠肽（ANP）以及血管扩张剂硝酸甘油和硝普钠，可降低培养的人内皮细胞基础状态下以及凝血酶刺激后的内皮素-1（ET-1）生成量，这是通过放射免疫测定法测得的。8-溴-3',5'-环磷酸鸟苷（cGMP）和罂粟碱也抑制ET-1的生成。因此，ANP和血管扩张剂对ET-1生成的抑制作用似乎是由鸟苷酸环化酶和cGMP介导的。ANP、硝普钠和硝酸甘油的部分血管舒张作用可能归因于对内皮ET-1生成的抑制。这可能是血管扩张剂参与血管张力调节的另一种机制。
