Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/handle/123456789/7487
Title: Antiarrhythmogenic effects of a neurotoxin from the spider Phoneutria nigriventer.
Authors: Almeida, Alvair Pinto de
Andrade, Alexandre Barbosa
Ferreira, Anderson José
Pires, Andrea Cristina Gomes
Damasceno, Dênis Derly
Alves, Márcia Netto Magalhães
Gomes, Enéas Ricardo de Morais
Kushmerick, Christopher
Lima, Ricardo de Freitas
Prado, Marco Antônio Maximo
Prado, Vânia Ferreira
Richardson, Michael
Cordeiro, Marta do Nascimento
Guatimosim, Silvia
Gomez, Marcus Vinicius
Keywords: Cardiac arrhythmias
Isolated heart
Atropine
Acetylcholine
Issue Date: 2011
Citation: ALMEIDA, A. P. de et al. Antiarrhythmogenic effects of a neurotoxin from the spider Phoneutria nigriventer. Toxicon, Oxford, v. 57, p. 217-224, 2011. Disponível em: <http://www.sciencedirect.com/science/article/pii/S0041010110004095>. Acesso em: 29 jan. 2017.
Abstract: In this study, we evaluated the effects of PhKv, a 4584 Da peptide isolated from the spider Phoneutria nigriventer venom, in the isolated rat heart and in isolated ventricular myocytes. Ventricular arrhythmias were induced by occlusion of the left anterior descending coronary artery for 15 min followed by 30 min of reperfusion. Administration of native PhKv (240 nM) 1 min before or after reperfusion markedly reduced the duration of arrhythmias. This effect was blocked by atropine, thereby indicating the participation of muscarinic receptors in the antiarrhythmogenic effect of PhKv. Notably, recombinant PhKv (240 nM) was also efficient to attenuate the arrhythmias (3.8 0.9 vs. 8.0 1.2 arbitrary units in control group). Furthermore, PhKv induced a significant reduction in heart rate. This bradycardia was partially blunted by atropine and potentiated by pyridostigmine. To further evaluate the participation of acetylcholine on the PhKv effects, we examined the release of this neurotransmitter from neuromuscular junctions. It was found that Phkv (200 nM) significantly increased the release of acetylcholine in this preparation. Moreover, PhKv (250 nM) did not cause any significant change in action potential or Ca2þ transient parameters in isolated cardiomyocytes. Altogether, these findings show an important acetylcholine-mediated antiarrhythmogenic effect of the spider PhKv toxin in isolated hearts.
URI: http://www.repositorio.ufop.br/handle/123456789/7487
metadata.dc.identifier.uri2: http://www.sciencedirect.com/science/article/pii/S0041010110004095
metadata.dc.identifier.doi: https://doi.org/10.1016/j.toxicon.2010.11.013
ISSN: 0041-0101
Appears in Collections:DEFAR - Artigos publicados em periódicos

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