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心房利钠肽、硝酸甘油和硝普钠可降低培养的内皮细胞基础状态及受刺激状态下的内皮素生成量。

Atrial natriuretic peptide, nitroglycerine, and nitroprusside reduce basal and stimulated endothelin production from cultured endothelial cells.

作者信息

Saijonmaa O, Ristimäki A, Fyhrquist F

机构信息

Unit of Clinical Physiology, Minerva Institute for Medical Research, Helsinki, Finland.

出版信息

Biochem Biophys Res Commun. 1990 Dec 14;173(2):514-20. doi: 10.1016/s0006-291x(05)80064-6.

Abstract

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.

摘要

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。

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