Zhao D, Tian Q, Zhao Y T, Gong C N, Han Q D, Zhang Z K, Tang J
Institute of Cardiovascular Research, Beijing Medical University.
Sheng Li Xue Bao. 1995 Jun;47(3):218-24.
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-Arginine. In addition, the vasodilator effect of AdM (13-52) disappeared with methylene blue (MB), which blocked cGMP formation. Using radioimmunoassay it was shown that 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.
在本研究中，对AdM（13 - 52）在大鼠体内外的降压机制进行了研究。发现一氧化氮合酶抑制剂L - NG - 硝基精氨酸（LNNA）可部分抑制AdM（13 - 52）的降压作用。AdM（13 - 52）的血管舒张作用依赖于血管内皮，并被LNNA以剂量依赖的方式抑制。这种LNNA诱导的抑制作用可用L - 精氨酸逆转。此外，亚甲蓝（MB）可消除AdM（13 - 52）的血管舒张作用，MB可阻断cGMP的形成。采用放射免疫分析法表明，LNNA降低了血管cGMP含量，但AdM（13 - 52）升高了血管cGMP含量，而联合应用AdM（13 - 52）和LNNA时血管cGMP含量未改变。上述结果提示，AdM（13 - 52）的血管舒张作用可能由一氧化氮介导。
