Navegando por Palavras-chave "Adenosine receptor"
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- ItemSomente MetadadadosThe A(1) receptor agonist R-Pia reduces the imbalance between cerebral glucose metabolism and blood flow during status epilepticus: Could this mechanism be involved with neuroprotection?(Elsevier B.V., 2011-01-01) Silva, Lara Ribeiro [UNIFESP]; Nehlig, Astrid; Rosim, Fernanda Elisa [UNIFESP]; Vignoli, Thiago [UNIFESP]; Persike, Daniele Suzete [UNIFESP]; Ferrandon, Arielle; Sinigaglia-Coimbra, Rita [UNIFESP]; Silva Fernandes, Maria Jose da [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ StrasbourgIt is well known that the uncoupling between local cerebral glucose utilization (LCGU) and local cerebral blood flow (LCBF), i.e. decrease in LCBF rates with high LCGU, is frequently associated with seizure-induced neuronal damage. This study was performed to assess if the neuroprotective effect of the adenosinergic A(1) receptor agonist R-N-phenylisopropyladenosine (R-Pia) injected prior to pilocarpine is able to reduce the uncoupling between LCGU and LCBF during status epilepticus (SE). Four groups of rats were studied: Saline, Pilo, R-Pia + Saline and R-Pia + Pilo. for LCGU and LCBF studies, rats were subjected to autoradiography using [C-14]-2-deoxyglucose and [C-14]-iodoantypirine, respectively. Radioligands were injected 4 h after SE onset. Neuronal loss was evaluated by Fluorojade-B (FJB) at two time points after SE onset (24 h and 7 days). the results showed a significant increase in LCGU in almost all brain regions studied in the Pilo and R-Pia + Pilo groups compared to controls. However, in R-Pia pretreated rats, the uncoupling between LCGU and LCBF was moderated in a limited number of structures as substantia nigra pars reticulata and hippocampal formation rather in favor of hyperperfusion. Significant increases in LCBF were observed in the entorhinal cortex, thalamic nuclei, mammillary body, red nucleus, zona incerta, pontine nucleus and visual cortex. the neuroprotective effect of R-Pia assessed by FJB showed a lower density of degenerating cells in the hippocampal formation, piriform cortex and basolateral amygdala. in conclusion our data shows that the neuroprotective effect of R-Pia was accompanied by a compensatory metabolic input in brain areas involved with seizures generation. Published by Elsevier Inc.
- ItemSomente MetadadadosThe association between caffeine consumption and objective sleep variables is dependent on ADORA2A c.1083T>C genotypes(Elsevier Science Bv, 2017) Nunes, Rafael Almeida [UNIFESP]; Mazzotti, Diego Robles [UNIFESP]; Hirotsu, Camila [UNIFESP]; Andersen, Monica L. [UNIFESP]; Tufik, Sergio [UNIFESP]; Bittencourt, Lia [UNIFESP]Objective: To verify the association between c.1083T>C polymorphism in the adenosine receptor A2A gene (ADORA2A) and objective sleep, as well as the correlation between caffeine consumption, sleep parameters, and electroencephalographic spectral power in a large, population-based sample from Sao Paulo, Brazil. Methods: This study was conducted in participants of the Sao Paulo Epidemiologic Sleep Study (EPISONO), a large, population-based survey consisting of a representative sample of the inhabitants of the city from Sao Paulo, Brazil, according to sex, age (20-80 years), and socioeconomic status in the year 2007. Questionnaires, polysomnography, spectral analysis of sleep electroencephalogram, and c.1083T>C polymorphism genotyping were performed in this study. Results: We found that caffeine consumption was positively correlated with sleep latency and a spectral power, as well as negatively correlated with percentage of N3 stage and delta spectral power in this stage. However, this association was identified only in T allele carriers and not in CC genotype. Conclusion: Our data support an important aspect of this polymorphism in ADORA2A gene, showing that the variant affects the association between caffeine consumption and objective sleep parameters in a large population-based cohort. (C) 2016 Elsevier B.V. All rights reserved.
- ItemSomente MetadadadosCardiac arrest induced by muscarinic or adenosine receptors agonists is reversed by DPCPX through double mechanism(Elsevier Science Bv, 2018) Camara, Henrique [UNIFESP]; da Silva Junior, Edilson Dantas [UNIFESP]; Garcia, Antonio G.; Jurkiewicz, Aron [UNIFESP]; Dantas Rodrigues, Juliano Quintella [UNIFESP]In the right atrium (RA), adenosine and acetylcholine inhibit the pacemaker function of the sinoatrial node and induce cardiac arrest. Pre-incubation of receptor antagonists is known to inhibit the cardiac arrest induced by these agonists
- ItemSomente MetadadadosIncreased Gi protein signaling potentiates the negative chronotropic effect of adenosine in the SHR right atrium(Springer, 2018) Rodrigues, Juliano Quintella Dantas [UNIFESP]; Camara, Henrique [UNIFESP]; Jurkiewicz, Aron [UNIFESP]|Godinho, Rosely Oliveira [UNIFESP]Hypertension is a risk factor for cardiovascular diseases, which have been associated with dysfunction of sympathetic and purinergic neurotransmission. Therefore, herein, we evaluated whether modifications of adenosine receptor signaling may contribute to the cardiac dysfunction observed in hypertension. Isolated right atria from spontaneously hypertensive (SHR) or normotensive Wistar rats (NWR) were used to investigate the influence of adenosine receptor signaling cascade in the cardiac chronotropism. Our results showed that adenosine, the endogenous agonist of adenosine receptors, and CPA, a selective agonist of A(1) receptor, decreased the atrial chronotropism of NWR and SHR in a concentration- and time-dependent manner, culminating in cardiac arrest (0 bpm). Interestingly, a 3-fold lower concentration of adenosine was required to induce the negative chronotropic effect in SHR atria. Pre-incubation of tissues from both strains with DPCPX, a selective A(1) receptor antagonist, inhibited the negative chronotropic effect of CPA, while simultaneous inhibition of A(2) and A(3) receptors, with ZM241385 and MRS1523, did not change the adenosine chronotropic effects. Moreover, 1 mu g/ml pertussis toxin, which inactivates the G alpha i protein subunit, reduced by 80% the negative chronotropic effects of adenosine in the NWR atrium, with minor effects in SHR tissue. These data indicate that the negative chronotropic effect of adenosine in right atrium depends exclusively on the activation of A(1) receptors. Moreover, the distinct responsiveness of NWR and SHR atria to pertussis toxin reveals that the enhanced negative chronotropic response of SHR right atrium is probably due to an increased activity of G alpha i protein-mediated.
- ItemAcesso aberto (Open Access)Papel da via extracelular AMP cíclico - adenosina na contração do músculo liso do trato respiratório(Universidade Federal de São Paulo (UNIFESP), 2017-11-30) Pacini, Enio Setsuo Arakaki [UNIFESP]; Godinho, Rosely Oliveira [UNIFESP]; http://lattes.cnpq.br/4929571824508354 ; http://lattes.cnpq.br/8042805299389223; Universidade Federal de São Paulo (UNIFESP)A adenosina 3’,5’-monofosfato cíclico (AMPc) é um segundo mensageiro intracelular universal que está envolvido em inúmeros processos biológicos, tais como a proliferação celular, transcrição gênica, transmissão neuronal e contração muscular. Também é conhecido o papel crucial do AMPc intracelular no relaxamento do músculo liso das vias aéreas desencadeado pela ativação de adrenoceptores (β2-AR) cujos agonistas são utilizados na clínica para o tratamento de doenças pulmonares inflamatórias como a asma e doenças pulmonares obstrutivas crônicas (DPOC). Além de sua função de sinalização intracelular clássica, o AMPc atua como um terceiro mensageiro extracelular em diversas células, na dependência do seu efluxo e conversão extracelular a AMP e adenosina, por ecto-fosfodiesterases e ecto-5'-nucleotidases, respectivamente. No entanto, a existência e a relevância funcional da chamada "via extracelular AMPc-adenosina" no músculo liso das vias aéreas ainda não foi descrita. Assim, nosso trabalho teve como objetivo identificar e caracterizar farmacologicamente o papel da via extracelular AMPc-adenosina na contração do músculo liso das vias aéreas. Através da quantificação intra- e extracelular de AMPc por imunoensaio (TR-FRET), demonstramos que a ativação de adrenoceptores β2 promove o efluxo de AMPc em traqueia isolada de rato. Demonstramos ainda que o AMPc extracelular é capaz de promover contração do músculo liso traqueal, e que o efeito contrátil induzido pelo AMPc exógeno depende da sua metabolização extracelular a adenosina e ativação de receptores A1. Além disso, dados preliminares indicam que a via extracelular AMPc-adenosina não influencia o relaxamento promovido por agonistas de adrenoceptores β em músculo traqueal de ratos normais. Devido à relevância dos receptores de adenosina na fisiopatologia da asma e DPOC, estabelecemos no laboratório o modelo de asma experimental em ratos Wistar. As traqueias provenientes de animais sensibilizados e desafiados com ovalbumina apresentaram hipercontratilidade em resposta ao AMPc extracelular quando comparada a resposta contrátil de tecido de animais controle. Os resultados apresentados nesse trabalho demonstram a existência da via extracelular AMPc-adenosina na via aérea de rato, a qual desempenha papel modulador na contração do músculo liso das vias aéreas.