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.