Possible involvement of adenine nucleotides in the neurotransmission of the mouse urinary bladder

Acevedo, C.G.; Contreras, Enrique

doi:10.1016/0742-8413(85)90176-8

Cited by 10 publications

(15 citation statements)

References 14 publications

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“…With this purpose, we characterized pharmacologically the mouse bladder responses to the exogenous application of ADO following transmural depolarization of bladder nerve terminals or the motor action of exogenous ATP. In addition, we tested for the existence of an ADO tone in the mouse bladder transmission, where our previous research revealed the participation of ATP as a neurotransmitter (Acevedo & Contreras, 1985;Acevedo et al, 1990).…”

Section: B)mentioning

confidence: 99%

“…The urinary bladder was removed, voided and immediately placed in Krebs-Ringer solution warmed at 370C and bubbled with 95% 02/5% CO2 to maintain a pH close to 7.4. The bladder was dissected from surrounding tissues; two transverse, incomplete cuts were performed which resulted in a thin muscle strip which was tied on both ends (Acevedo & Contreras, 1985). One extreme was fixed to a hook on the 12 ml tissue chamber, the other was connected to a Grass force displacement transducer (FT 03C) in order to record isometric contractions.…”

Section: Bioassay and Quantification Of Drug Effectsmentioning

confidence: 99%

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Pharmacological characterization of adenosine A₁ and A₂ receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Acevedo

Contreras

Escalona

et al. 1992

British J Pharmacology

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1 The nerve-evoked contractions elicited by transmural electrical stimulation of mouse urinary bladders superfused in modified Krebs Ringer buffer containing 1 IAM atropine plus 3.4 IBM guanethidine were inhibited by adenosine (ADO) and related nucleoside analogues with the following rank order of potency: R-phenylisopropyladenosine (R-PIA) > cyclohexyladenosine (CHA) > 5'N-ethylcarboxamido adenosine (NECA) > ADO > S-phenylisopropyladenosine (S-PIA). Tissue preincubation with 8-phenyltheophylline (8-PT) displaced to the right, in a parallel fashion, the NECA concentration-response curve.2 The contractions elicited by application of exogenous adenosine 5'-triphosphate (ATP) were also inhibited by ADO and related structural analogues. The rank order of potency to reduce the motor response to ATP was: NECA > 2-chloroadenosine (CADO) > R-PIA > ADO > CHA > S-PIA. 3 The ADO-induced ATP antagonism was of a non-competitive nature and was not specific. Tissue incubation with 10 AM NECA not only reduced the motor responses elicited by ATP, but also 5-hydroxytryptamine, acetylcholine and prostaglandin F2CK. The action of NECA was antagonized following tissue preincubation with 8-PT. The inhibitory action of NECA was not mimicked by 10 gM CHA. 4 The maximal bladder ATP contractile response was significantly increased by tissue preincubation with 5-30 gM 8-PT. 5 The 0.15 Hz evoked muscular twitch was significantly increased by 8-PT while dipyridamole consistently reduced the magnitude of the twitch response. These results are consonant with the hypothesis that an endogenous ADO tone modulates the bladder neurotransmission. 6 A working model is proposed suggesting the presence of ADO-Al and A2 receptors in the mouse urinary bladder. The A1 receptor subpopulation is probably of presynaptic origin whereas the smooth muscle membranes contain a population of the A2 receptor subtype.

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Section: B)mentioning

confidence: 99%

Section: Bioassay and Quantification Of Drug Effectsmentioning

confidence: 99%

Pharmacological characterization of adenosine A₁ and A₂ receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Acevedo

Contreras

Escalona

et al. 1992

British J Pharmacology

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“…In the vas deferens, ET-1 also facilitates neurotransmission, potentiating ATP, but not the noradrenalineinduced contractions . The ATP receptors in the bladder are Pu in nature, as indicated by the order of potency of several nucleotides: AMP-CPP> AMP-PCP> AMP-PNP> ATP> 2-Me-S-ATP> ADP (Acevedo & Contreras, 1985;Donoso et al, unpublished observations). The similarity between the facilitation of the nerve-evoked contractions and that elicited by exogenous ATP suggests that the ET-1-induced effect involves, at least in part, the participation of endogenous ATP as a bladder transmitter.…”

Section: Discussionmentioning

confidence: 99%

“…Adult male Sprague Dawley rats (250-300 g), raised in our Animal Reproduction Laboratories, were killed by cervical dislocation; the abdominal cavity was opened, the bladder was mechanically voided, excised from surrounding tissues, and mounted in a bath for the recording of isometric contractions as detailed by Acevedo & Contreras (1985). Unless otherwise specified, the composition of the incubation buffer was (mM): NaCl 118, KCl 5.4, CaC12 2.5, KH2PO4 1.2, MgSO4 1.2, NaHCO323.8, glucose 11.1, atropine 0.001 and guanethidine 0.0034.…”

Section: Bioassaymentioning

confidence: 99%

“…The most solid evidence supporting ATP as a neurotransmitter is derived from investigations in the vas deferens (Fedan et al, 1981;Meldrum & Burnstock, 1983;Sneddon & Burnstock, 1984;Sneddon & Westfall, 1984;Stjmrne & Astrand, 1984), the mesenteric artery (Ramme et al, 1987), and the rat bladder (Burnstock et al, 1978b;Kasakov & Burnstock, 1983;Hoyle & Burnstock, 1985;Acevedo & Contreras 1985).…”

Section: Introductionmentioning

confidence: 99%

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Involvement of ET_A receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder

Donoso

Salas

Sepulveda

et al. 1994

British J Pharmacology

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1 Endothelin-1 (ET-1; 3-10 nM) raised the tone of rat bladders bathed in buffer containing atropine (1 gtM) plus guanethidine (3.4 JAM). In addition, ET-1 potentiated, in a concentration-dependent fashion (1-10 nM), the contractions evoked by both transmural nerve stimulation and applications of exogenous adenosine 5'-triphosphate (ATP). 2 The threshold concentration of ET-1 required to facilitate non-adrenergic non-cholinergic (NANC) transmission and potentiate ATP-induced contractions, was about 10 fold lower than that required to increase the bladder tone (3 nM). 3 The ET-1-induced increase in basal tension reached its maximal effect within 60-90 s. In contrast, the 7.8 JAM ATP-induced contractions increased by 50% within the first minute following incubation with 1O nM ET-1 but required about 5 min to develop the maximal effect. 4 The ET-1-induced potentiation of NANC or ATP responses was long-lasting and persisted in spite of extensive washing. The recovery of the bladder excitability depended on the concentration of ET-1. Following the application of 3 nM ET-1, recovery required 30 min; applications of 10 nM ET-1 required at least 60 min for full recovery. 5The ET-1-induced potentiation of responses was selective for ATP and related structural analogues.ET-1 did not modify the contractions induced by acetylcholine, 5-hydroxytryptamine, prostaglandin F2, or bradykinin. 6 The potency of ET-2 was similar to that of ET-1. ET-3 and ET-C-terminal hexapeptide were inactive up to 100 M. Sarafotoxin S6b was 2 to 3 fold less potent than ET-1 whereas sarafotoxin S6c (100 nM) was inactive. AGETB-9 and AGETB-89, two ETB receptor agonists, were also inactive (up to 100 nM). 7 Removal of one or both disulphide bonds in ET-1 and tryptophan-21 formylation of ET-1, resulted in inactive peptides (up to 100 nM). 8 The ET-1 receptor antagonists, BE-18257B and FR 139317, blocked both the ET-1-induced rise in tone and the potentiation of ATP responses in a concentration-dependent fashion. FR 139317 was at least 30 fold more potent than BE-18257B. Both antagonists blocked at lower concentrations the ET-l increase in bladder tone as compared to the ATP potentiation. The antagonism was slowly reversible. 9 Results are consistent with the presence of ETA receptors in the rat bladder, which mediate both actions of ET-1. The interaction of ET-1 with purinergic mechanisms is discussed.

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The effects of Ins2(Akita) diabetes and chronic angiotensin II infusion on cystometric properties in mice

Dolber

Jin

Nassar

et al. 2013

Neurourol. Urodynam.

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Aims Diabetes is associated with both dysfunction of the lower urinary tract (LUT) and overactivity of the renin-angiotensin system (RAS). Although it is well known that the RAS affects normal LUT function, very little is known about RAS effects on the diabetic LUT. Accordingly, we investigated the effects of chronic angiotensin II (AngII) treatment on the LUT in a model of type 1 diabetes. Methods Ins2(Akita) diabetic mice (20 wk old) and their age-matched background controls underwent conscious cystometric evaluation after 4 wk of chronic AngII treatment (700 ng/kg/min by osmotic pump) or vehicle (saline). Results Diabetic mice had compensated LUT function with bladder hypertrophy. Specifically, micturition volume, residual volume and bladder capacity were all increased, while voiding efficiency and pressure generation were unchanged as bladder mass, contraction duration, and phasic urethral function were increased. AngII significantly increased voiding efficiency and peak voiding pressure and decreased phasic frequency irrespective of diabetic state and, in diabetic but not normoglycemic control mice, significantly decreased residual volume and increased contraction duration and nonphasic contraction duration. Conclusions The Ins2(Akita) diabetic mice had compensated LUT function at 20 wk of age. Even under these conditions, AngII had beneficial effects on LUT function, resulting in increased voiding efficiency. Future studies should therefore be conducted to determine whether AngII can rescue the decompensated LUT function occurring in end-stage diabetic uropathy.

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Possible involvement of adenine nucleotides in the neurotransmission of the mouse urinary bladder

Cited by 10 publications

References 14 publications

Pharmacological characterization of adenosine A₁ and A₂ receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Pharmacological characterization of adenosine A₁ and A₂ receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Involvement of ET_A receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder

The effects of Ins2(Akita) diabetes and chronic angiotensin II infusion on cystometric properties in mice

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Possible involvement of adenine nucleotides in the neurotransmission of the mouse urinary bladder

Cited by 10 publications

References 14 publications

Pharmacological characterization of adenosine A1 and A2 receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Pharmacological characterization of adenosine A1 and A2 receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Involvement of ETA receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder

The effects of Ins2(Akita) diabetes and chronic angiotensin II infusion on cystometric properties in mice

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Pharmacological characterization of adenosine A₁ and A₂ receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Pharmacological characterization of adenosine A₁ and A₂ receptors in the bladder: evidence for a modulatory adenosine tone regulating non‐adrenergic non‐cholinergic neurotransmission

Involvement of ET_A receptors in the facilitation by endothelin‐1 of non‐adrenergic non‐cholinergic transmission in the rat urinary bladder