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使用拮抗剂来鉴定介导α,β-亚甲基腺苷5'-三磷酸使大鼠离体迷走神经去极化的受体。

The use of antagonists to characterize the receptors mediating depolarization of the rat isolated vagus nerve by alpha, beta-methylene adenosine 5'-triphosphate.

作者信息

Trezise D J, Kennedy I, Humphrey P P

机构信息

Glaxo Institute of Applied Pharmacology, Department of Pharmacology, University of Cambridge.

出版信息

Br J Pharmacol. 1994 May;112(1):282-8. doi: 10.1111/j.1476-5381.1994.tb13065.x.

Abstract
  1. We have previously found that the P2x-purinoceptor agonist, alpha, beta-methylene adenosine 5'-triphosphate (alpha, beta-methylene ATP), depolarizes the rat cervical vagus nerve, measured with a 'grease-gap' extracellular recording technique. This effect was attenuated by the P2 purinoceptor antagonist, suramin. In the present study we have investigated in more detail the antagonism produced by suramin and have also investigated the actions of two other putative P2 purinoceptor antagonists, cibacron blue and pyridoxal-phosphate-6-azophenyl-2', 5'-disulphonic acid (iso-PPADS). Furthermore, we have studied the interactions between suramin and cibacron blue or iso-PPADS in an attempt to determine whether these antagonists act at a common receptor site. 2. Suramin (1 x 10(-5)-1 x 10(-4) M) produced reversible, concentration-related rightward displacements of the concentration-effect curve to alpha, beta-methylene ATP. Schild analysis of this antagonism yielded a pA2 value of 5.90 with a slope value of 0.47. 3. Cibacron blue (3 x 10(-5)-1 x 10(-4) M) also antagonized depolarizations induced by alpha, beta-methylene ATP. The antagonistic effects of cibacron blue were slow to reach equilibrium but could be readily reversed on washout. At low concentrations for antagonism, cibacron blue (1 x 10(-5) M and 3 x 10(-5) M) produced enhancement of the maximal response to alpha, beta-methylene ATP. At the highest concentration tested (1 x 10(-4) M) the concentration-effect curve to alpha, beta-methylene ATP was shifted to the right in a parallel manner, yielding a pKB estimate of 4.96. 4. Iso-PPADS (1 X 10-6 1 X 10-5- M) produced a concentration-related depression in the maxima ofthe concentration-effect curves to alpha,beta-methylene ATP. Analysis of these data by a double reciprocal plot yielded a pKB estimate of 6.02. This profile of insurmountable antagonism could not be attributed to irreversible binding of iso-PPADS to the receptor since the effect of iso-PPADS could be reversed on washing, albeit slowly.5. In the presence of suramin (1 x 10-4 M), cibacron blue (1 x 10-4 M) produced no further rightward displacement of the alpha,beta-methylene ATP concentration-effect curve. The mean agonist concentration ratios in the presence of suramin or cibacron blue alone (11.7 and 10.3, respectively) were not significantly different from the mean concentration-ratio in the presence of both antagonists (11.8). This finding suggests that high concentrations of alpha,beta-methylene ATP activate a receptor population which is resistant to blockade by either antagonist.6. The antagonistic effect of iso-PPADS (1 x 10-5 M) was partially attenuated by suramin (1I x 10-4 M).It is possible that this interaction reflects a slow dissociation of iso-PPADS from the receptor with which suramin and alpha,beta-methylene ATP interact.7. Suramin, cibacron blue or iso-PPADS had no marked effect on depolarization produced by 5-hydroxytryptamine (5-HT, 1 x 10-7-3 x 10-5 M), indicating their specificity in antagonizing responses to alpha, beta-methylene ATP.8. Responses to alpha,beta-methylene ATP were not antagonized by 8-para-sulphophenyltheophylline (3 x 10-5M), ondansetron (1 x 10-7 M), bicuculline (1 x I0-5 M), phentolamine (1 X 10-6 M) or hexamethonium(1 X 10-4 M), which are antagonists at P1-purinoceptors, 5-HT3 receptors, GABAA receptors, a-adrenoceptors and nicotinic cholinoceptors, respectively, thereby excluding the involvement of these receptors.Indomethacin (3 X 10-6 M) had no effect on responses to alpha,beta-methylene ATP.9. The results obtained with three purinoceptor antagonists confirm and extend our original supposition that alpha,beta-methylene ATP-induced depolarization of the rat vagus nerve is mediated predominantly via P2 purinoceptors, thought to be of the P2,X subtype. The finding that responses induced by high concentrations of agonist were resistant to blockade by suramin and cibacron blue, but could be attenuated by iso-PPADS, adds further weight to our speculation that the purinoceptor population in the rat vagus nerve is heterogeneous.
摘要
  1. 我们先前发现,P2x嘌呤受体激动剂α,β-亚甲基腺苷5'-三磷酸(α,β-亚甲基ATP)可使大鼠颈迷走神经去极化,这是通过“油脂间隙”细胞外记录技术测得的。P2嘌呤受体拮抗剂苏拉明可减弱这种效应。在本研究中,我们更详细地研究了苏拉明产生的拮抗作用,还研究了另外两种假定的P2嘌呤受体拮抗剂——汽巴克隆蓝和磷酸吡哆醛-6-偶氮苯-2',5'-二磺酸(异-PPADS)的作用。此外,我们研究了苏拉明与汽巴克隆蓝或异-PPADS之间的相互作用,以试图确定这些拮抗剂是否作用于共同的受体位点。2. 苏拉明(1×10⁻⁵ - 1×10⁻⁴ M)使α,β-亚甲基ATP的浓度-效应曲线产生可逆的、浓度相关的右移。对这种拮抗作用进行Schild分析,得到的pA2值为5.90,斜率值为0.47。3. 汽巴克隆蓝(3×10⁻⁵ - 1×10⁻⁴ M)也拮抗α,β-亚甲基ATP诱导的去极化。汽巴克隆蓝的拮抗作用达到平衡较慢,但冲洗后可迅速逆转。在低浓度拮抗时,汽巴克隆蓝(1×10⁻⁵ M和3×10⁻⁵ M)增强了对α,β-亚甲基ATP的最大反应。在测试的最高浓度(1×10⁻⁴ M)时,α,β-亚甲基ATP的浓度-效应曲线以平行方式右移,得到的pKB估计值为4.96。4. 异-PPADS(1×10⁻⁶ - 1×10⁻⁵ M)使α,β-亚甲基ATP的浓度-效应曲线的最大值产生浓度相关的降低。通过双倒数作图分析这些数据,得到的pKB估计值为6.02。这种不可逾越的拮抗作用特征不能归因于异-PPADS与受体的不可逆结合,因为异-PPADS的作用虽然缓慢,但冲洗后可以逆转。5. 在存在苏拉明(1×10⁻⁴ M)的情况下,汽巴克隆蓝(1×10⁻⁴ M)未使α,β-亚甲基ATP浓度-效应曲线进一步右移。单独存在苏拉明或汽巴克隆蓝时的平均激动剂浓度比(分别为11.7和10.3)与两种拮抗剂同时存在时的平均浓度比(11.8)无显著差异。这一发现表明,高浓度的α,β-亚甲基ATP激活了一个对两种拮抗剂的阻断均有抗性的受体群体。6. 异-PPADS(1×10⁻⁵ M)的拮抗作用被苏拉明(1×10⁻⁴ M)部分减弱。这种相互作用可能反映了异-PPADS从与苏拉明和α,β-亚甲基ATP相互作用的受体上缓慢解离。7. 苏拉明、汽巴克隆蓝或异-PPADS对5-羟色胺(5-HT,1×10⁻⁷ - 3×10⁻⁵ M)产生的去极化无明显影响,表明它们在拮抗对α,β-亚甲基ATP的反应方面具有特异性。8. 8-对磺基苯甲基黄嘌呤(3×10⁻⁵ M)、昂丹司琼(1×10⁻⁷ M)、荷包牡丹碱(1×10⁻⁵ M)、酚妥拉明(1×10⁻⁶ M)或六甲铵(1×10⁻⁴ M)对α,β-亚甲基ATP的反应无拮抗作用,它们分别是P1嘌呤受体、5-HT3受体、GABAA受体、α-肾上腺素能受体和烟碱型胆碱能受体的拮抗剂,从而排除了这些受体的参与。吲哚美辛(3×10⁻⁶ M)对α,β-亚甲基ATP的反应无影响。9. 三种嘌呤受体拮抗剂获得的结果证实并扩展了我们最初的推测,即α,β-亚甲基ATP诱导的大鼠迷走神经去极化主要通过P2嘌呤受体介导,该受体被认为是P2X亚型。高浓度激动剂诱导的反应对苏拉明和汽巴克隆蓝的阻断具有抗性,但可被异-PPADS减弱这一发现,进一步支持了我们关于大鼠迷走神经中嘌呤受体群体是异质性的推测。

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