PHARMACOLOGICAL CHARACTERIZATION OF ADENOSINE-A1 AND A2 RECEPTORS IN THE BLADDER - EVIDENCE FOR A MODULATORY ADENOSINE TONE REGULATING NONADRENERGIC NONCHOLINERGIC NEUROTRANSMISSION

dc.contributor.authorACEVEDO, CG
dc.contributor.authorCONTRERAS, E
dc.contributor.authorESCALONA, J
dc.contributor.authorLEWIN, J
dc.contributor.authorHUIDOBROTORO, JP
dc.date.accessioned2025-01-23T19:22:03Z
dc.date.available2025-01-23T19:22:03Z
dc.date.issued1992
dc.description.abstract1 The nerve-evoked contractions elicited by transmural electrical stimulation of mouse urinary bladders superfused in modified Krebs Ringer buffer containing 1-mu-M atropine plus 3.4-mu-M guanethidine were inhibited by adenosine (ADO) and related nucleoside analogues with the following rank order of potency: RB-phenylisopropyladenosine (RB-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.
dc.description.abstract2 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) > RB-PIA > ADO > CHA > S-PIA.
dc.description.abstract3 The ADO-induced ATP antagonism was of a non-competitive nature and was not specific. Tissue incubation with 10-mu-m NECA not only reduced the motor responses elicited by ATP, but also 5-hydroxytryptamine, acetylcholine and prostaglandin F2-alpha. The action of NECA was antagonized following tissue preincubation with 8-PT. The inhibitory action of NECA was not mimicked by 10-mu-m CHA.
dc.description.abstract4 The maximal bladder ATP contractile response was significantly increased by tissue preincubation with 5-30-mu-m 8-PT.
dc.description.abstract5 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.
dc.description.abstract6 A working model is proposed suggesting the presence of ADO-A1 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.
dc.fuente.origenWOS
dc.identifier.issn0007-1188
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/98946
dc.identifier.wosidWOS:A1992JK06700020
dc.issue.numero1
dc.language.isoen
dc.pagina.final126
dc.pagina.inicio120
dc.revistaBritish journal of pharmacology
dc.rightsacceso restringido
dc.subjectNONNORADRENERGIC NONCHOLINERGIC NEUROTRANSMISSION
dc.subjectPURINERGIC TRANSMISSION
dc.subjectADENOSINE RECEPTORS
dc.subjectADENOSINE A1, A2 MECHANISMS
dc.subjectADENOSINE MODULATION
dc.subjectURINARY BLADDER
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titlePHARMACOLOGICAL CHARACTERIZATION OF ADENOSINE-A1 AND A2 RECEPTORS IN THE BLADDER - EVIDENCE FOR A MODULATORY ADENOSINE TONE REGULATING NONADRENERGIC NONCHOLINERGIC NEUROTRANSMISSION
dc.typeartículo
dc.volumen107
sipa.indexWOS
sipa.trazabilidadWOS;2025-01-12
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