Effects Of Beta-adrenoceptor Antagonists In The Neural Nitric Oxide Release Induced By Electrical Field Stimulation And Sodium Channel Activators In The Rabbit Corpus Cavernosum.

dc.creatorTeixeira, Cleber E
dc.creatorBaracat, Juliana S
dc.creatorArantes, Eliane C
dc.creatorDe Nucci, Gilberto
dc.creatorAntunes, Edson
dc.date2005-Sep
dc.date2015-11-27T13:02:19Z
dc.date2015-11-27T13:02:19Z
dc.date.accessioned2018-03-29T01:01:13Z
dc.date.available2018-03-29T01:01:13Z
dc.identifierEuropean Journal Of Pharmacology. v. 519, n. 1-2, p. 146-53, 2005-Sep.
dc.identifier0014-2999
dc.identifier10.1016/j.ejphar.2005.07.011
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/16084509
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/196362
dc.identifier16084509
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1296595
dc.descriptionBeta-Adrenoceptor antagonists may present receptor-independent mechanisms, such as blockade of voltage-gated sodium channels. This study aimed to investigate the effects of non-selective (propranolol), and selective beta1- (atenolol, metoprolol and betaxolol) and beta2-adrenoceptor (ICI 118,551) antagonists in the nitric oxide (NO)-mediated rabbit corpus cavernosum relaxations induced by either electrical field stimulation (EFS) or activators of voltage-gated sodium channels. The sodium channel blockers tetrodotoxin and saxitoxin abolished the relaxations induced by EFS or sodium channel activators of binding site-2 (aconitine and veratridine), site-3 (Ts3 toxin), site-4 (Ts1 toxin) and site-5 (brevetoxin-3). The beta-adrenoceptor antagonists failed to affect the relaxations induced by EFS, aconitine and veratridine. Relaxations induced by Ts3 and Ts1 toxins, as well as brevetoxin-3, were markedly reduced by prior addition of propranolol, betaxolol and ICI 118,551. During the established relaxation induced by Ts3 toxin, propranolol failed to restore the basal tone. In conclusion, beta-adrenoceptor antagonists may cause an allosteric inhibition at the binding site-3, -4 and -5 of voltage-gated sodium channels, leading to blockade of neural NO release.
dc.description519
dc.description146-53
dc.languageeng
dc.relationEuropean Journal Of Pharmacology
dc.relationEur. J. Pharmacol.
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAconitine
dc.subjectAdrenergic Beta-antagonists
dc.subjectAnimals
dc.subjectAtenolol
dc.subjectBetaxolol
dc.subjectBinding Sites
dc.subjectElectric Stimulation
dc.subjectIn Vitro Techniques
dc.subjectInsect Proteins
dc.subjectMale
dc.subjectMetoprolol
dc.subjectMuscle Relaxation
dc.subjectNeurotoxins
dc.subjectNitric Oxide
dc.subjectPenis
dc.subjectPropanolamines
dc.subjectPropranolol
dc.subjectRabbits
dc.subjectSaxitoxin
dc.subjectScorpion Venoms
dc.subjectSodium Channel Agonists
dc.subjectTetrodotoxin
dc.subjectVeratridine
dc.titleEffects Of Beta-adrenoceptor Antagonists In The Neural Nitric Oxide Release Induced By Electrical Field Stimulation And Sodium Channel Activators In The Rabbit Corpus Cavernosum.
dc.typeArtículos de revistas


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