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首页> 外文期刊>Basic & clinical pharmacology & toxicology. >Assessment and characterization of purinergic contractions and relaxations in the rat urinary bladder.
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Assessment and characterization of purinergic contractions and relaxations in the rat urinary bladder.

机译:大鼠膀胱中嘌呤能收缩和松弛的评估和表征。

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The aim of the present study was to assess the purinoceptor functional responses of the urinary bladder by using isolated rat urinary bladder strip preparations. ATP elicited a transient bladder contraction followed by a sustained relaxation and ADP, UDP and UTP generated predominantly potent relaxations (relaxatory potencies: ADP = ATP > UDP = UTP). The ATP contractions were desensitized with the P2X(1/3) purinoceptor agonist/desensitizer alpha,beta-meATP and reduced by the P2 purinoceptor antagonist PPADS but unaffected by the P2 purinoceptor antagonist suramin. Electrical field stimulation (1-60 Hz) evoked frequency-dependent bladder contractions that were decreased by incubation with alpha,beta-meATP but not further decreased by PPADS. Suramin antagonized relaxations generated by UDP but not those by ADP, ATP or UTP. PPADS antagonized and tended to antagonize UTP and UDP relaxations, respectively, but did neither affect ADP nor ATP relaxations. ADP relaxations were insensitive to the P2Y(1) purinoceptor antagonist MRS 2179 and the ATP-sensitive potassium channel antagonist glibenclamide. The ATP relaxations were inhibited by the P1 purinoceptor antagonist 8-p-sulfophenyltheophylline but unaffected by the A2A adenosine receptor antagonist 8-(3-chlorostyryl)caffeine and glibenclamide. Adenosine evoked relaxations that were antagonized by the A2B adenosine receptor antagonist PSB 1115. Thus, in the rat urinary bladder purinergic contractions are elicited predominantly by stimulation of the P2X(1) purinoceptors, while UDP/UTP-sensitive P2Y purinoceptor(s) and P1 purinoceptors of the A2B adenosine receptor subtype are involved in bladder relaxation.
机译:本研究的目的是通过使用分离的大鼠膀胱剥离制剂来评估膀胱的嘌呤受体功能反应。 ATP引起短暂的膀胱收缩,然后持续舒张,而ADP,UDP和UTP主要产生强效舒张作用(松弛潜能:ADP = ATP> UDP = UTP)。 ATP收缩用P2X(1/3)嘌呤受体激动剂/脱敏剂α,β-meATP脱敏,并通过P2嘌呤受体拮抗剂PPADS降低,但不受P2嘌呤受体拮抗剂suramin的影响。电场刺激(1-60 Hz)引起了频率依赖性膀胱收缩,与α,β-meATP孵育可降低膀胱收缩,但PPADS则不会进一步降低。苏拉明拮抗UDP产生的松弛,但不抑制ADP,ATP或UTP产生的松弛。 PPADS分别拮抗并趋向于对抗UTP和UDP弛豫,但均不影响ADP和ATP弛豫。 ADP放松对P2Y(1)嘌呤受体拮抗剂MRS 2179和ATP敏感钾通道拮抗剂格列本脲不敏感。 ATP松弛被P1嘌呤受体拮抗剂8-p-磺基苯基茶碱抑制,但不受A2A腺苷受体拮抗剂8-(3-氯苯乙烯基)咖啡因和格列本脲影响。腺苷引起的松弛被A2B腺苷受体拮抗剂PSB 1115拮抗。因此,在大鼠膀胱中,嘌呤能收缩主要通过刺激P2X(1)嘌呤受体而引起,而UDP / UTP敏感的P2Y嘌呤受体和P1引起。 A2B腺苷受体亚型的嘌呤受体与膀胱松弛有关。

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