Kromer W
Department of Pharmacology, Byk Gulden, Konstanz, Germany.
Life Sci. 1993;53(13):1061-8. doi: 10.1016/0024-3205(93)90259-6.
The present voltage-clamp data from guinea pig colonic mucosa indicate that mu opioid receptors both enhance and inhibit net chloride secretion stimulated by PGE1 plus theophylline. Actually, enhancement by the mu opioid agonist DAGO (0.2 nmol/l) declines and finally turns into inhibition with increasing net chloride secretion observed in control preparations taken from the same animals. Moreover, inhibition by the mu opioid antagonist CTOP-NH2 (100 nmol/l) increases with increasing inhibition (or decreasing enhancement) by the mu opioid agonist DAGO. Thus, the mu opioid agonist DAGO and the mu opioid antagonist CTOP-NH2 display opposite effects on net chloride secretion only to a limited degree but otherwise show parallel, either stimulatory or inhibitory, effects. To explain this complex function of mu opioid receptors in the control of net chloride secretion, a working hypothesis is being proposed.
来自豚鼠结肠黏膜的当前电压钳数据表明,μ阿片受体既能增强也能抑制由前列腺素E1加茶碱刺激引起的净氯分泌。实际上,在取自同一动物的对照制剂中,随着观察到的净氯分泌增加,μ阿片激动剂DAGO(0.2 nmol/l)的增强作用下降,最终转变为抑制作用。此外,μ阿片拮抗剂CTOP-NH2(100 nmol/l)的抑制作用随着μ阿片激动剂DAGO抑制作用的增强(或增强作用的减弱)而增加。因此,μ阿片激动剂DAGO和μ阿片拮抗剂CTOP-NH2仅在有限程度上对净氯分泌表现出相反的作用,但在其他方面表现出平行的、刺激或抑制的作用。为了解释μ阿片受体在控制净氯分泌中的这种复杂功能,正在提出一个工作假设。