α-Adrenoceptor-mediated prejunctional effects of chloroethylclonidine in the canine saphenous vein

dc.contributorUniversidade Estadual Paulista (UNESP)
dc.creatorGuimarães, Serafim
dc.creatorPaiva, Maria Q.
dc.creatorPereira, Oduvaldo
dc.date2014-05-27T11:18:15Z
dc.date2016-10-25T18:14:35Z
dc.date2014-05-27T11:18:15Z
dc.date2016-10-25T18:14:35Z
dc.date1997-09-01
dc.date.accessioned2017-04-06T00:50:07Z
dc.date.available2017-04-06T00:50:07Z
dc.identifierJournal of Pharmacology and Experimental Therapeutics, v. 282, n. 3, p. 1326-1330, 1997.
dc.identifier0022-3565
dc.identifierhttp://hdl.handle.net/11449/65177
dc.identifierhttp://acervodigital.unesp.br/handle/11449/65177
dc.identifier2-s2.0-0030886329
dc.identifierhttp://jpet.aspetjournals.org/content/282/3/1326.full.pdf
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/886926
dc.descriptionThe present study was undertaken to look for the effect of chloroethylclonidine (CEC) on prejunctional alpha-2 autoreceptors of the canine saphenous vein. The effect was tested on tritium overflow evoked by electrical stimulation from tissues preloaded with 0.2 μM 3H- norepinephrine. Yohimbine (3-300 nM) and CEC (1-125 μM) increased and UK- 14,304 reduced the overflow of tritium evoked by 300 pulses (1 Hz). The maximal increase of tritium overflow caused by yohimbine was much higher than that caused by CEC: 3.82 and 1.74 times, respectively. CEC (5 μM) abolished both the inhibition caused by UK-14,304 and the enhancement of tritium overflow caused by yohimbine. However, when CEC was added after yohimbine, it reduced the electrically evoked overflow of tritium, the maximal effect being a reduction of tritium overflow by 35%. Prazosin (1-100 nM) did not change either the inhibitory effect of UK-14,304 or the facilitatory effect of CEC. These results suggest that CEC acts on two different subtypes of prejunctional alpha-2 autoreceptors; on one of them it acts as an antagonist and increases the electrically evoked overflow of tritium (and inhibits both the effect of UK-14,304 and yohimbine); on the other it acts as an agonist and reduces the electrically evoked overflow of tritium. Alternatively, one can admit that CEC is able to inhibit alpha-2 autoreceptors, which causes an increase of the transmitter release, and to activate a nonadrenergic inhibitory receptor thus causing a reduction of the transmitter release.
dc.languageeng
dc.relationJournal of Pharmacology and Experimental Therapeutics
dc.rightsinfo:eu-repo/semantics/closedAccess
dc.subjectalpha adrenergic receptor
dc.subjectbrimonidine
dc.subjectchloroethylclonidine
dc.subjecttritium
dc.subjectyohimbine
dc.subjectanimal tissue
dc.subjectcontrolled study
dc.subjectdog
dc.subjectdrug effect
dc.subjectdrug mechanism
dc.subjectelectrostimulation therapy
dc.subjectevoked response
dc.subjectfemale
dc.subjectmale
dc.subjectneurotransmission
dc.subjectnonhuman
dc.subjectpresynaptic nerve
dc.subjectpriority journal
dc.subjectsaphenous vein
dc.subjectAdrenergic alpha-Antagonists
dc.subjectAnimals
dc.subjectAutoreceptors
dc.subjectClonidine
dc.subjectDogs
dc.subjectDose-Response Relationship, Drug
dc.subjectFemale
dc.subjectMale
dc.subjectPrazosin
dc.subjectQuinoxalines
dc.subjectReceptors, Adrenergic, alpha-2
dc.subjectSaphenous Vein
dc.subjectYohimbine
dc.titleα-Adrenoceptor-mediated prejunctional effects of chloroethylclonidine in the canine saphenous vein
dc.typeOtro


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