Hársing L G, Rónai A Z, Somogyi G T, Umezawa H, Bajusz S, Vizi E S
J Auton Pharmacol. 1984 Mar;4(1):33-43. doi: 10.1111/j.1474-8673.1984.tb00431.x.
The effect of the opioid heptapeptide Met5-enkephalin-Arg6-Phe7 was measured on the contractions of the longitudinal muscle of the guinea-pig ileum and mouse vas deferens; on release of endogenous and newly synthesized acetylcholine from the longitudinal muscle strip preparation of the guinea-pig ileum and of 3H-noradrenaline from mouse vas deferens. Met5-enkephelin-Arg6-Phe7 depressed the contractions of the longitudinal muscle strip of guinea-pig ileum elicited by low frequency stimulation (IC50 366.5 +/- 71.5 nM). The Ke value of naltrexone against the heptapeptide was found to be 0.50 +/- 0.08 nM. Bestatin prolonged and strongly potentiated the action of the opioid peptide in this tissue while captopril proved to be only slightly effective. Met5-enkephalin-Arg6-Phe7 also inhibited neuroeffector transmission in the mouse vas deferens with an IC50 value of 9.44 +/- 2.24 nM. The Ke value of naltrexone was 6.33 +/- 1.22 nM against the heptapeptide. Met5-enkephalin-Arg6-Phe7 (10(-5) M) failed to affect the low frequency stimulated release of endogenous acetylcholine from the guinea-pig ileum preparation. Addition of either bestatin or captopril with the heptapeptide resulted in a reduction of acetylcholine output. The opioid peptide by itself decreased the release of newly synthesized acetylcholine outflow from this organ. Met5-enkephalin-Arg6-Phe7 also reduced the 3H-noradrenaline outflow from mouse vas deferens and this effect was antagonized by naltrexone. From our data we conclude that Met5-enkephalin-Arg6-Phe7 affects the neural transmission of peripheral autonomically innervated organs by depressing the release of neurotransmitter. In vitro it has enkephalin-like character with a preference for the so called delta receptor interaction.
研究了阿片类七肽甲硫氨酸脑啡肽-精氨酸6-苯丙氨酸7对豚鼠回肠和小鼠输精管纵肌收缩的影响；对豚鼠回肠纵肌条制剂中内源性和新合成的乙酰胆碱释放以及小鼠输精管中3H-去甲肾上腺素释放的影响。甲硫氨酸脑啡肽-精氨酸6-苯丙氨酸7抑制低频刺激引起的豚鼠回肠纵肌条收缩（IC50为366.5±71.5 nM）。发现纳曲酮对该七肽的Ke值为0.50±0.08 nM。贝司他汀延长并强烈增强了该阿片肽在该组织中的作用，而卡托普利仅显示出轻微效果。甲硫氨酸脑啡肽-精氨酸6-苯丙氨酸7也抑制小鼠输精管中的神经效应传递，IC50值为9.44±2.24 nM。纳曲酮对该七肽的Ke值为6.33±1.22 nM。甲硫氨酸脑啡肽-精氨酸6-苯丙氨酸7（10⁻⁵ M）未能影响豚鼠回肠制剂中低频刺激引起的内源性乙酰胆碱释放。将贝司他汀或卡托普利与该七肽一起添加会导致乙酰胆碱释放量减少。该阿片肽本身可减少该器官新合成的乙酰胆碱流出量。甲硫氨酸脑啡肽-精氨酸6-苯丙氨酸7还减少了小鼠输精管中3H-去甲肾上腺素的流出量，且该效应被纳曲酮拮抗。根据我们的数据，我们得出结论，甲硫氨酸脑啡肽-精氨酸6-苯丙氨酸7通过抑制神经递质释放来影响外周自主神经支配器官的神经传递。在体外，它具有脑啡肽样特性，更倾向于与所谓的δ受体相互作用。
