Relaxation Of Rabbit Corpus Cavernosum By Selective Activators Of Voltage-gated Sodium Channels: Role Of Nitric Oxide-cyclic Guanosine Monophosphate Pathway.

dc.creatorFernandes de Oliveira, Juliano
dc.creatorTeixeira, Cleber E
dc.creatorArantes, Eliane C
dc.creatorde Nucci, Gilberto
dc.creatorAntunes, Edson
dc.date2003-Sep
dc.date2015-11-27T12:52:23Z
dc.date2015-11-27T12:52:23Z
dc.date.accessioned2018-03-29T00:57:55Z
dc.date.available2018-03-29T00:57:55Z
dc.identifierUrology. v. 62, n. 3, p. 581-8, 2003-Sep.
dc.identifier1527-9995
dc.identifier
dc.identifierhttp://www.ncbi.nlm.nih.gov/pubmed/12946781
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/195506
dc.identifier12946781
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1295739
dc.descriptionTo investigate the capacity of voltage-gated Na(+) channel activators such as batrachotoxin, aconitine, veratridine, Ts1 (formerly Tityus gamma-toxin), and brevetoxin-3 to induce relaxation of rabbit isolated corpus cavernosum (RbCC) and the pharmacologic mechanisms underlying this phenomenon. The voltage-gated Na(+) channels of the corpus cavernosum are essential for erectile function. A number of biologic toxins exert their effects by modifying the properties of these channels. Male New Zealand white rabbits were anesthetized with pentobarbital sodium. Strips of RbCC were transferred to 10-mL organ baths containing oxygenated and warmed Krebs solution. The RbCC strips were connected to force-displacement transducers, and changes in isometric force were recorded using a PowerLab 400 data acquisition system. Corporeal smooth muscle was precontracted submaximally with phenylephrine (10 micromol/L). The binding site-2 (batrachotoxin, aconitine, and veratridine) and binding site-5 (brevetoxin-3) voltage-gated Na(+) channel activators caused slow-onset RbCC relaxations, and the binding site-4 activator Ts1 produced transitory relaxations followed by a return to baseline. The Na(+)channel blockers tetrodotoxin and saxitoxin (0.1 micromol/L each) abolished the relaxations induced by these agonists. Similarly, the nitric oxide synthase inhibitor N(omega)-nitro-l-arginine methyl ester (100 micromol/L) markedly reduced the relaxations and l-arginine (1 mmol/L) restored the relaxations. The soluble guanylyl cyclase inhibitor 1H-[1,2,4] oxidiazolo[4,3-alpha] quinoxalin-1-one (10 micromol/L) reduced the relaxations, and the phosphodiesterase type 5 inhibitor sildenafil (100 nmol/L) significantly potentiated the relaxations by all activators. Our results indicate that the relaxations evoked by selective activators of voltage-gated Na(+) channels are mediated by the release of nitric oxide from nitrergic nerves and the activation of the nitric oxide-cyclic guanosine monophosphate pathway in the smooth muscle cells of erectile tissue.
dc.description62
dc.description581-8
dc.languageeng
dc.relationUrology
dc.relationUrology
dc.rightsfechado
dc.rights
dc.sourcePubMed
dc.subjectAconitine
dc.subjectAnimals
dc.subjectArginine
dc.subjectBatrachotoxins
dc.subjectBinding Sites
dc.subjectCyclic Gmp
dc.subjectGuanylate Cyclase
dc.subjectIn Vitro Techniques
dc.subjectInsect Proteins
dc.subjectIsometric Contraction
dc.subjectMale
dc.subjectMarine Toxins
dc.subjectMuscle, Smooth
dc.subjectNg-nitroarginine Methyl Ester
dc.subjectNeurotoxins
dc.subjectNitric Oxide
dc.subjectNitric Oxide Synthase
dc.subjectOxocins
dc.subjectPenile Erection
dc.subjectPenis
dc.subjectPiperazines
dc.subjectPurines
dc.subjectRabbits
dc.subjectScorpion Venoms
dc.subjectSodium Channel Agonists
dc.subjectSodium Channel Blockers
dc.subjectSodium Channels
dc.subjectSulfones
dc.subjectVeratridine
dc.titleRelaxation Of Rabbit Corpus Cavernosum By Selective Activators Of Voltage-gated Sodium Channels: Role Of Nitric Oxide-cyclic Guanosine Monophosphate Pathway.
dc.typeArtículos de revistas


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