P2 受体激动剂对大鼠离体肛尾肌交感神经效应器传递的影响。

Effects of P2-receptor agonists on sympathetic neuroeffector transmission in the rat isolated anococcygeus muscle.

作者信息

Najbar-Kaszkiel A T, Rand M J

机构信息

Department of Medical Laboratory Science, RMIT University, Melbourne, VIC, Australia.

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1998 May;357(5):519-25. doi: 10.1007/pl00005202.

DOI:10.1007/pl00005202

PMID:9650804

Abstract

The effects of nicotinamide adenine dinucleotide phosphate (NADPH), alpha,beta-methylene adenosine 5'-triphosphate (alpha,beta-MeATP), L-beta,gamma-methylene adenosine 5'-triphosphate (L-beta,gamma-MeATP), 2-methylthio-adenosine 5'-triphosphate (MeSATP) and adenosine-5-O-(2'-thiodiphosphate) (ADPbetaS) were investigated on the contractions to electrical field stimulation in the rat anococcygeus muscle. Stimulation-induced contractions were not affected by L-beta,gamma-MeATP (3-100 microM) or MeSATP (3-100 microM), but were enhanced by NADPH (10-100 microM), alpha,beta-MeATP (3-30 microM) and ADPbetaS (3-10 microM) in a concentration-dependent manner, and the enhancements were antagonised by the P2-receptor antagonist suramin (100 microM). The enhancement produced by alpha,beta-MeATP (10 microM) and ADPbetaS (10 microM) was also antagonised by pyridoxal-phosphate-6-azophenyl-2',4'-disulphonic acid (10 microM) and reactive blue 2 (100 microM). The enhancement produced by alpha,beta-MeATP (10 microM) was not altered by NG-nitro-L-arginine methyl ester (100 microM), desipramine (1 microM) or idazoxan (0.1 microM) excluding, respectively, the possible involvement of nitric oxide, neuronal amine uptake or alpha2-autoinhibition of noradrenergic transmission. Contractions elicited by low (0.1 and 0.3 microM) but not by higher (1 and 3 microM) concentrations of exogenously applied noradrenaline were enhanced by alpha,beta-MeATP (10 microM). Neither the resting nor the stimulation-induced effluxes of radioactivity from [3H]-noradrenaline-labelled anococcygeus muscles were affected by alpha,beta-MeATP (10-100 microM). The findings suggest that P2-receptors subserve the enhancing actions of NADPH, alpha,beta-MeATP and ADPbetaS on sympathetic neuroeffector transmission; however, the subtype of P2-receptor involved and its location remain unclear.

摘要

研究了烟酰胺腺嘌呤二核苷酸磷酸（NADPH）、α,β-亚甲基腺苷5'-三磷酸（α,β-MeATP）、L-β,γ-亚甲基腺苷5'-三磷酸（L-β,γ-MeATP）、2-甲硫基腺苷5'-三磷酸（MeSATP）和腺苷-5-O-(2'-硫代二磷酸)（ADPβS）对大鼠肛门尾骨肌电场刺激收缩的影响。L-β,γ-MeATP（3-100微摩尔）或MeSATP（3-100微摩尔）对刺激诱导的收缩无影响，但NADPH（10-100微摩尔）、α,β-MeATP（3-30微摩尔）和ADPβS（3-10微摩尔）以浓度依赖性方式增强收缩，且P2受体拮抗剂苏拉明（100微摩尔）可拮抗这种增强作用。α,β-MeATP（10微摩尔）和ADPβS（10微摩尔）产生的增强作用也被磷酸吡哆醛-6-偶氮苯基-2',4'-二磺酸（10微摩尔）和活性蓝2（100微摩尔）拮抗。α,β-MeATP（10微摩尔）产生的增强作用不受NG-硝基-L-精氨酸甲酯（100微摩尔）、地昔帕明（1微摩尔）或咪唑克生（0.1微摩尔）的影响，分别排除了一氧化氮、神经元胺摄取或去甲肾上腺素能传递的α2-自身抑制可能的参与。低浓度（0.1和0.3微摩尔）而非高浓度（1和3微摩尔）外源性去甲肾上腺素引起的收缩被α,β-MeATP（10微摩尔）增强。α,β-MeATP（10-100微摩尔）对[3H]-去甲肾上腺素标记的肛门尾骨肌的静息或刺激诱导的放射性流出均无影响。这些发现表明，P2受体参与了NADPH、α,β-MeATP和ADPβS对交感神经效应器传递的增强作用；然而，所涉及的P2受体亚型及其位置仍不清楚。