Miller L, Rance M J, Shaw J S, Traynor J R
Eur J Pharmacol. 1985 Oct 8;116(1-2):159-63. doi: 10.1016/0014-2999(85)90197-9.
The inhibitory action of dynorphin-(1-9) on the electrically stimulated mouse vas deferens was seen to be antagonised by the delta-selective opioid antagonist ICI 174864. The observed delta-receptor mediated responses were partially, but not totally, prevented by peptidase inhibitors which protect the C- and N-termini of dynorphin-(1-9). [3H]Dynorphin-(1-9) is rapidly degraded by slices of vasa deferentia of the mouse. The major product of this metabolism co-elutes with [Leu5]enkephalin on reverse phase HPLC. It is concluded that a major component of the inhibitory effects of dynorphin-(1-9) on the mouse vas deferens is mediated by degradation to [Leu5]enkephalin which in turn acts through delta-receptors. It is possible that in other in vitro and in vivo systems, the effects produced by dynorphin-(1-9) might be similarly mediated by delta-receptor activation.
强啡肽-(1-9)对电刺激的小鼠输精管的抑制作用可被δ-选择性阿片样物质拮抗剂ICI 174864拮抗。观察到的δ-受体介导的反应可被保护强啡肽-(1-9)的C端和N端的肽酶抑制剂部分但非完全阻断。[3H]强啡肽-(1-9)可被小鼠输精管切片迅速降解。这种代谢的主要产物在反相高效液相色谱上与[亮氨酸5]脑啡肽共洗脱。得出的结论是,强啡肽-(1-9)对小鼠输精管抑制作用的主要成分是通过降解为[亮氨酸5]脑啡肽来介导的,而[亮氨酸5]脑啡肽又通过δ-受体起作用。在其他体外和体内系统中,强啡肽-(1-9)产生的效应可能同样由δ-受体激活介导。