Navegando por Autor "Guatimosim, Silvia"
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Item Antiarrhythmogenic effects of a neurotoxin from the spider Phoneutria nigriventer.(2011) 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 ViniciusIn 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.Item Basal and β-Adrenergic cardiomyocytes contractility dysfunction induced by dietary protein restriction is associated with downregulation of SERCA2a expression and disturbance of endoplasmic reticulum Ca2+ regulation in rats.(2014) Penitente, Arlete Rita; Novaes, Rômulo Dias; Silva, Marcelo Eustáquio; Silva, Márcia Ferreira da; Quintão Júnior, Judson Fonseca; Guatimosim, Silvia; Cruz, Jader dos Santos; Chianca Júnior, Deoclécio Alves; Natali, Antônio José; Neves, Clóvis AndradeBackground: The mechanisms responsible for the cardiac dysfunction associated with dietary protein restriction (PR) are poorly understood. Thus, this study was designed to evaluate the effects of PR on calcium kinetics, basal and β-adrenergic contractility in murine ventricular cardiomyocytes. Methods: After breastfeeding male Fisher rats were distributed into a control group (CG, n = 20) and a protein-restricted group (PRG, n = 20), receiving isocaloric diets for 35 days containing 15% and 6% protein, respectively. Biometric and hemodynamic variables were measured. After euthanasia left ventricles (LV) were collected for histopathological evaluation, SERCA2a expression, cardiomyocytes contractility and Ca2+ sparks analysis. Results: PRG animals showed reduced general growth, increased heart rate and arterial pressure. These animals presented extracellular matrix expansion and disorganization, cardiomyocytes hypotrophy, reduced amplitudes of shortening and maximum velocity of contraction and relaxation at baseline and after β-adrenergic stimulation. Reduced SERCA2a expression as well as higher frequency and lower amplitude of Ca2+ sparks were observed in PRG cardiomyocytes. Conclusion: The observations reveal that protein restriction induces marked myocardial morphofunctional damage. The pathological changes of cardiomyocyte mechanics suggest the potential involvement of the β-adrenergic system, which is possibly associated with changes in SERCA2a expression and disturbances in Ca2+ intracellular kinetics.Item Ketamine potentiates TRPV1 receptor signaling in the peripheral nociceptive pathways.(2020) Costa, Flavia Lage Pessoa da; Pinto, Mauro Cunha Xavier; Astoni, Duana Carvalho dos Santos; Carobin, Natália Virtude; Jesus, Itamar Couto Guedes de; Ferreira, Luana Assis; Guatimosim, Silvia; Silva, Juliana Figueira; Castro Junior, Célio José deTRPV1 is a cation channel expressed in peripheral nociceptive pathways and its activation can trigger noci- ception signals to the brain. Ketamine is an intravenous anesthetic routinely used for anesthesia induction and with potent analgesic activity. Despite its proven depressant action on peripheral sensory pathways, the re- lationship between ketamine and TRPV1 receptors is still unclear. In this study, we evaluated the effect of ketamine injected peripherally in a rat model of spontaneous pain induced by capsaicin. We also investigated the effect of ketamine on Ca2+ transients in cultured dorsal root ganglia (DRG) neurons and HEK293 cells expressing the TRPV1 receptor (HEK-TRPV1 cells). Intraplantar administration of ketamine caused an unexpected increase in nocifensive behavior induced by capsaicin. Incubation of HEK-TRPV1 cells with 10 μM ketamine increased TRPV1 and PKCє phosphorylation. Ketamine potentiated capsaicin-induced Ca2+ transients in HEK-TRPV1 cells and DRG neurons. Ketamine also prevented TRPV1 receptor desensitization induced by successive applications of capsaicin. єV1-2, a PKCє inhibitor, reduced potentiation of capsaicin-induced Ca2+ transients by ketamine. Taken together, our data indicate that ketamine potentiates TRPV1 receptor sensitivity to capsaicin through a mechanism dependent on PKCє activity.