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 a,b-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 a,b-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.The contraction of the urinary bladder depends mainly on the parasympathetic stimulation of the muscarinic receptors populating the detrusor [1]. However, as early as 1895 Langley described that a certain part of the contractile response of the bladder is resistant to atropine [2]. It was later suggested that other transmitters besides acetylcholine and noradrenaline contribute to the regulation of the urinary bladder function, and adenosine-5¢-triphosphate (ATP) was identified as one of these transmitters [3]. ATP generates a transient contraction caused by the stimulation of the P2X purinoceptors causing depolarization through non-selective cation channels [4]. Of the seven known homomeric P2X purinoceptor subtypes, the P2X 1 subtype has been shown to occur in the smooth muscle of the rat bladder [5]. It has also been demonstrated that the P2X 1 subtype is the predominant purinoceptor present in the human bladder [6]. Following the ATP-generated contraction, a sustained relaxation occurs, which has been suggested to depend on the metabolite of ATP, adenosine, stimulating inhibitory P1 purinoceptors [3,7]. Others have attributed the relaxation to the direct action of ATP at G-protein-coupled P2Y purinoceptors [8,9].The present study was undertaken to further investigate and characterize the functional responses of the purinoceptors in the normal rat urinary bladder. Th...

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In the current study we show that stimulation of afferents at one side of the bladder induces, via impulses from the central nervous system, contractions from the other side. This novel model enables quantitative comparisons of changes occurring within the micturition reflex arc in bladder disorders. Neurourol. Urodynam. 33:550-557, 2014. © 2013 Wiley Periodicals, Inc.

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