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胍基丁胺在离体豚鼠乳头肌的电生理效应 总被引:2,自引:0,他引:2
应用细胞内微电极技术,观察了胍基丁胺(agmatine,AGM)对豚鼠乳头肌细胞的电生理效应。结果表明:(1)AGM浓度依赖地缩短正常乳头肌动作电位的时程;(2)对部分去极化的乳头肌,AGM(1mmol/L)除缩短动作电位时程外,还抑制动作电位零相最大上升速度,并降低其幅值和超射值;(3)预先应用一氧化氮合酶抑制剂LNAME(05mmol/L),不能影响AGM(1mmol/L)的电生理效应;(4)预先应用咪唑啉受体(imidazolinereceptor,IR)和α2肾上腺素能受体(alpha2adrenergicreceptor,α2AR)拮抗剂idazoxan(01mmol/L),则可完全阻断AGM(1mmol/L)的电生理效应。以上结果提示,AGM对乳头肌的电生理效应似由α2AR和IR介导,并与胞浆内Ca2+减少有关。 相似文献
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M.F Heath R.W Farndale C.S Napthine L.J Hayes R.J Evans 《Comparative biochemistry and physiology. Part B, Biochemistry & molecular biology》1997,118(4):889-893
Adrenaline is a weak aggregating agonist for human platelets acting through G-protein-coupled α2-adrenoceptors to inhibit adenylate cyclase and thus reduce cyclic AMP levels. Studies of equine platelets have shown that adrenaline is unable to promote their aggregation. We now confirm that adrenaline is without effect on equine platelet aggregation and demonstrate that it is also without effect on equine platelet membrane adenylate cyclase activity. We have previously shown that equine platelet membranes contain conventionally regulated adenylate cyclase activity, with both stimulatory ligands (forskolin and PGE1) and inhibitory ligands (collagen and PAF) each showing substantial and dose-dependent effects. We now show, in Western blots, that equine platelet membranes contain G proteins, including Gi2 (which mediates inhibition of adenylate cyclase by adrenaline in human platelets), Gi3, Gs, and Gq. Hence, all the necessary components and responses are in place in equine platelets to provide for a conventional role for cyclic AMP and adenylate cyclase in modulating platelet aggregation. The basis for the failure of adrenaline, unlike other ligands, to deliver such a signal, appears to be a marked lack of α2-adrenoceptors. This is supported by the low receptor density we found in idazoxan binding studies. 相似文献
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l ‐DOPA‐induced dyskinesia is characterised by debilitating involuntary movement, which limits quality of life in patients suffering from Parkinson’s disease. Here, we investigate effects of the α2 adrenoceptor antagonist idazoxan on l ‐DOPA‐induced dyskinesia as well as on alterations of extracellular l ‐DOPA and dopamine (DA) levels in the striatum in dyskinetic rats. Male Wistar rats were unilaterally lesioned with 6‐hydroxydopamine and subsequently treated with l ‐DOPA/benserazide to induce stable dyskinetic movements. Administration of idazoxan [(9 mg/kg, intraperitoneal (i.p.)] significantly alleviated l ‐DOPA‐induced dyskinesia, whereas idazoxan (3 mg/kg, i.p.) did not affect dyskinetic behaviour. Bilateral in vivo microdialysis revealed that idazoxan 9 mg/kg reduces extracellular peak l ‐DOPA levels in the lesioned and intact striatum as well as DA levels in the lesioned striatum. In parallel, the exposure to idazoxan in the striatum was monitored. Furthermore, no idazoxan and l ‐DOPA drug–drug interaction was found in plasma, brain tissue and CSF. In conclusion, the decrease of l ‐DOPA‐derived extracellular DA levels in the lesioned striatum significantly contributes to the anti‐dyskinetic effect of idazoxan. 相似文献
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