肾上腺髓质素（13－52）降压机制的探讨

A STUDY ON HYPOTENSIVE MECHANISM OF ADRENOMEDULLIN (13-52)

本工作在整体和离体大鼠模型上观察研究了肾上腺髓质素（１３－５２）［ＡｄＭ（１３－５２）］的降压机制，发现ＡｄＭ（１３－５２）的降压作用可被一氧化氮合酶（ＮＯＳ）的竟争性桔抗剂Ｌ－ＮＧ－硝基－精氨酸（ＬＮＮＡ）部分抑制；ＡｄＭ（１３－５２）的舒血管作用依赖于血管内皮并可被ＬＮＮＡ抑制，且具有剂量效应关系，ＬＮＮＡ的这种效应可被Ｌ－精氨酸（Ｌ－Ａｒｇ）逆转；用亚甲蓝（ＭＢ）阻断血管内的环－磷酸鸟苷酸（ｃＧＭＰ），则导致ＡｄＭ（１３－５２）的舒血管作用消失；放免测定显示ＬＮＮＡ可以降低血管内ｃＧＭＰ含量，而ＡｄＭ（１３－５２）则使后者含量增加，这一现象在ＡｄＭ（１３－５２）与ＬＮＮＡ合用时消失。实验结果提示，ＡｄＭ（１３－５２）的舒血管降血压效应与ＮＯ有关，可能是通过ＮＯ介导的。

In the present study the hypotensive mechanism of AdM (13-52) was investigated in rats, both in vitro and in vivo. It was found that the hypotensive effect of AdM (13-52) could be partially inhibited by L-NG-nitro-arginine (LNNA), an inhibitor of nitric oxide synthase. The vasodilator effect of AdM (13-52) was dependent on vascular endothelium and inhibited by LNNA in a dose-dependent manner. This LNNA induced inhibitory effect could be reversed with L-Asginine. In addition, the vasodilator effect of AdM (13-52) disappeared with methylene blue (MB), which blocked cGMP formation.Using radioimmunoassay it was Shown thst LNNA lowered, but AdM (13-52) elevated the vascular cGMP content, while vascular cGMP content was not altered by co-application of AdM (13-52) and LNNA. The above results suggest that the vasodilator effect of AdM (13-52) might be mediated by nitric oxide.