Inoue S, Bian K, Okamura T, Okunishi H, Toda N
Department of Pharmacology, Shiga University of Medical Sciences, Japan.
Jpn J Pharmacol. 1989 Jul;50(3):271-82. doi: 10.1254/jjp.50.271.
Effects of eperisone, an antispasmodic in skeletal muscle, were investigated in helical strips of dog saphenous artery and vein. Eperisone relaxed saphenous arteries and veins previously contracted with norepinephrine, serotonin, acetylcholine, K+, or Ba2+; but in contrast, it produced contractions in the blood vessels contracted with prostaglandin (PG) F2 alpha. Treatment with eperisone attenuated the contractions induced by norepinephrine and serotonin in the arteries and those by clonidine and phenylephrine in the veins. Eperisone inhibited angiotensin II-induced relaxations, mediated possibly by endogenous PGI2, but did not alter relaxations caused by exogenous PGI2. Treatment with eperisone (10(-5) M) potentiated the contractile response to electrical stimulation of adrenergic nerves; the potentiating effect was suppressed by yohimbine. The eperisone-induced contraction in PGF2 alpha-contracted arteries was inhibited by treatment with indomethacin or aspirin, although cyclooxygenase activity was not inhibited by eperisone. These results may indicate that eperisone blocks postjunctional alpha 1- and alpha 2-adrenergic, muscarinic, serotonergic receptors and prejunctional alpha 2 adrenoceptors and reduces PGI2 synthesis via a mechanism other than cyclooxygenase inhibition.
在犬隐动脉和静脉螺旋条上研究了骨骼肌解痉药乙哌立松的作用。乙哌立松可使先前用去甲肾上腺素、5-羟色胺、乙酰胆碱、钾离子或钡离子收缩的隐动脉和静脉舒张；但相反，它可使用前列腺素（PG）F2α收缩的血管产生收缩。乙哌立松处理减弱了去甲肾上腺素和5-羟色胺在动脉中以及可乐定和去氧肾上腺素在静脉中所诱导的收缩。乙哌立松抑制了可能由内源性前列环素（PGI2）介导的血管紧张素II诱导的舒张，但不改变外源性PGI2引起的舒张。用乙哌立松（10^(-5) M）处理增强了对肾上腺素能神经电刺激的收缩反应；育亨宾可抑制这种增强作用。尽管乙哌立松不抑制环氧化酶活性，但用吲哚美辛或阿司匹林处理可抑制乙哌立松在PGF2α收缩的动脉中所诱导的收缩。这些结果可能表明，乙哌立松可阻断节后α1和α2肾上腺素能、毒蕈碱能、5-羟色胺能受体以及节前α2肾上腺素能受体，并通过一种不同于抑制环氧化酶的机制减少PGI2的合成。
