Navegando por Autor "Campos, Danilo Roman"
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Item Dysautonomia due to reduced cholinergic neurotransmission causes cardiac remodeling and heart failure.(2010) Gomes, Aline Alves Lara; Damasceno, Dênis Derly; Pires, Rita Gomes Wanderley; Gros, Robert; Gomes, Enéas Ricardo de Morais; Gavioli, Mariana; Lima, Ricardo de Freitas; Guimarães, Diogo Aparecido da Silva; Lima, Patrícia Maria d'Almeida; Bueno Júnior, Carlos Roberto; Vasconcelos, Anilton Cesar; Campos, Danilo Roman; Menezes, Cristiane Alves da Silva; Sirvente, Raquel de Assis; Salemi, Vera Maria Cury; Mady, Charles; Caron, Marc G.; Ferreira, Anderson José; Brum, Patricia Chakur; Resende, Rodrigo Ribeiro; Cruz, Jader dos Santos; Gomez, Marcus Vinicius; Prado, Vânia Ferreira; Almeida, Alvair Pinto de; Prado, Marco Antônio Maximo; Fonseca, Silvia Carolina GuatimosimOverwhelming evidence supports the importance of the sympathetic nervous system in heart failure. In contrast, much less is known about the role of failing cholinergic neurotransmission in cardiac disease. By using a unique genetically modified mouse line with reduced expression of the vesicular acetylcholine transporter (VAChT) and consequently decreased release of acetylcholine, we investigated the consequences of altered cholinergic tone for cardiac function. M-mode echocardiography, hemodynamic experiments, analysis of isolated perfused hearts, and measurements of cardiomyocyte contraction indicated that VAChT mutant mice have decreased left ventricle function associated with altered calcium handling. Gene expression was analyzed by quantitative reverse transcriptase PCR and Western blotting, and the results indicated that VAChT mutant mice have profound cardiac remodeling and reactivation of the fetal gene program. This phenotype was attributable to reduced cholinergic tone, since administration of the cholinesterase inhibitor pyridostigmine for 2 weeks reversed the cardiac phenotype in mutant mice. Our findings provide direct evidence that decreased cholinergic neurotransmission and underlying autonomic imbalance cause plastic alterations that contribute to heart dysfunction.Item The positive inotropic effect of the ethyl acetate fraction from Erythrina velutina leaves on the mammalian myocardium : the role of adrenergic receptors.(2013) Passos, Amilton Gustavo da Silva; Gondim, Antônio Nei Santana; Campos, Danilo Roman; Cruz, Jader dos Santos; Garcia, Eduardo Antônio Conde; Araújo Neto, Vitor; Estevam, Charles dos Santos; Cerqueira, Sandra Valéria Santos; Brandão, Geraldo Célio; Oliveira, Alaíde Braga de; Vasconcelos, Carla Maria Lins deObjectives We studied the effects of ethyl acetate fraction (EAcF) obtained from Erythrina velutina leaves on mammalian myocardium. Methods The effect of EAcF on the contractility was studied using guinea-pig left atria mounted in a tissue bath (Tyrode’s solution, 29°C, 95% CO2, 5% O2) and electrically stimulated (1 Hz). Concentration-response curves of EAcF were obtained in the presence of propranolol (1 mm), nifedipine (1 mm) and in reserpinized animals (5 mg/kg). The involvement of l-type calcium current (ICa,L) on the EAcF effect was observed in cardiomyocytes of mice assessed using patch-clamp technique. Key findings EAcF (550 mg/ml) had a positive inotropic effect, increasing the atrial force by 164% (EC50 = 157 44 mg/ml, n = 6), but it was less potent than isoproterenol (EC50 = 0.0036 0.0019 mg/ml, n = 8). The response evoked by EAcF was abolished by propranolol or nifedipine. Reserpine did not alter the inotropic response of EAcF. Furthermore, an enhancement of the ICa,L peak (31.2%) with EAcF was observed. Chemical analysis of EAcF revealed the presence of at least 10 different flavonoid glycoside derivatives. Two were identified as vicenin II and isorhoifolin. Conclusions We conclude that EAcF increases the cardiac contractile force by increasing the l-type calcium current and activating the adrenergic receptor pathway.