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Id: biblio-1089607
Autor: Zhang, Jianfeng; Hu, Guojin; Yang, Shengyong.
Título: Intracoronary sarcoplasmic reticulum calcium-atpase gene therapy in advanced heart failure patients with reduced ejection fraction: a prospective cohort study
Fonte: Clinics;75:e1530, 2020. tab, graf.
Idioma: en.
Resumo: OBJECTIVE: Heart failure is a progressive and debilitating disease. Intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy may improve the function of cardiac muscle cells. This study aimed to test the hypothesis that intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy can improve outcomes and reduce the number of recurrent and terminal events in advanced heart failure patients with reduced ejection fraction. METHODS: A total of 768 heart failure patients with reduced ejection fraction and New York Heart Association classification II to IV were included in this prospective cohort study. Patients either underwent intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy (CA group, n=384) or received oral placebo (PA group; n=384). Data regarding recurrent and terminal event(s), treatment-emergent adverse effects, and outcome measures were collected and analyzed. RESULTS: After a follow-up period of 18 months, intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy reduced the number of hospital admissions (p=0.001), ambulatory treatments (p=0.0004), and deaths (p=0.024). Additionally, intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy improved the left ventricular ejection fraction (p<0.0001) and Kansas City Cardiomyopathy Questionnaire score (p<0.0001). The number of recurrent and terminal events/patients were higher in the PA group than in the CA group after the follow-up period of 18 months (p=0.015). The effect of the intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy was independent of the confounding variables. No new arrhythmias were reported in the CA group. CONCLUSIONS: Intracoronary sarcoplasmic reticulum calcium-ATPase gene therapy reduces the number of recurrent and terminal events and improves the clinical course of advanced heart failure patients with reduced ejection fraction.
Descritores: Retículo Sarcoplasmático
Insuficiência Cardíaca
-Volume Sistólico
Terapia Genética
Cálcio
Estudos Prospectivos
Função Ventricular Esquerda
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático
Limites: Humanos
Masculino
Feminino
Responsável: BR1.1 - BIREME


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Id: biblio-1095107
Autor: Márquez-Orozco, Amalia; De la Fuente-Juárez, Graciela; Márquez-Orozco, María Cristina.
Título: El Diazepam altera la ultraestructura del atrio fetal de ratón / Diazepam alters the ultrastructure of fetal atrium in rat
Fonte: Int. j. med. surg. sci. (Print);3(4):991-996, dic. 2016. ilus.
Idioma: es.
Resumo: El diazepam (DZ) es un tranquilizante menor sintético, utilizado en pacientes con trastornos psicológicos y psiquiátricos. Es sedante, miorrelajante, anticonvulsionante y antipsicótico. El DZ atraviesa la barrera placentaria humana y la del ratón. Mujeres jóvenes que son adictas al fármaco, si se embarazan y continúan utilizándolo, sobre todo durante el primer trimestre, exponen a sus hijos a presentar alteraciones psicomotoras. El propósito de este trabajo fue investigar si el DZ administrado durante la gestación,induce alteraciones ultraestructurales del miocardio fetal de ratón. El grupo (DZ) de hembras gestantes deratón de la cepa CD-1 fue tratado con dosis únicas diarias de 1,0 mg/kg/pc/sc del día 6 al 17 y un grupo (C)que recibió solución salina. El día 18 las hembras de ambos grupos se anestesiaron, los fetos se perfundieron por vía intracardiaca con paraformaldehído al 1 % y glutaraldehido al 2,5 %, se les extrajo el corazón, se disecó el atrio, se fijó en OsO4 al 1 % y se incluyó en resina epóxica. Los cortes finos se contrastaron conacetato de uranilo y citrato de plomo y se observaron en un microscopio electrónico de transmisión. En los miocitos de los fetos del grupo DZ las sarcómeras del miocardio compacto tenían menor longitud que las del grupo C. Se observaron zonas con miofibrillas desorganizadas. El retículo sarcoplásmico de algunos miocitos presentaba cisternas distendidas y fragmentadas, mitocondrias alteradas y se observaron abundantes polirribosomas. Los cambios podrían deberse al efecto del DZ sobre la síntesis de actina y miosina pesada y sobre los organelos citoplásmicos, mediados por receptores benzodiazepínicos periféricos presentes en la membrana externa de las mitocondrias y asociados a canales de calcio dependientes de voltaje. Las alteraciones ultraestructurales del miocardio atrial de fetos de ratones expuestos in utero a DZ podrían tener efectos posnatales.

Diazepam (DZ) is a syntheticminor tranquilizer, used in patients with psychologicaland psychiatric disorders. It is a relaxing sedative,anticonvulsant and antipsychotic. DZ crosses thehuman placental barrier in mouse. Young women who are addicted to the drug, if they become pregnantand continue to use it, particularly during the firsttrimester, expose their children to psychomotor disorders. The purpose of this study was to investigate whether DZ administered during pregnancy induces ultrastructural alterations of fetal mouse myocardium.The group (DZ) of pregnant female mice of the CD-1strain was treated with a single daily dose of 1.0 mg/ kg / pc / sc of day 6 to 17 and a group (C) that received saline solution. On day 18 females of bothgroups were anesthetized, the fetuses were perfusedby intracardiac route with 1 % paraformaldehyde and 2.5 % glutaraldehyde, the heart was removed, theatrium was dissected, fixed in 1 % OsO4, it wasimmersed in epoxy resin. The fine sections werecontrasted with uranyl acetate and lead citrate and observed in a transmission electron microscope. Inthe myocytes of the fetuses of the DZ group, the sarcomers of the compact myocardium were shorter than those of the C group. Areas with disorganized myofibrils were observed. The sarcoplasmic reticulumof some myocytes had distended and fragmented 996cisterns, altered mitochondria, and abundant polyribosomes were observed. The changes may bedue to the effect of DZ on the synthesis of actin and heavy myosin and on cytoplasmic organelles mediatedby peripheral benzodiazepine receptors present onthe outer membrane of the mitochondria and associated with voltage-dependent calcium channels.Ultrastructural alterations of the atrial myocardium of fetuses of mice exposed to DZ in utero may have postnatal effects.
Descritores: Diazepam/toxicidade
Coração Fetal/efeitos dos fármacos
-Retículo Sarcoplasmático/efeitos dos fármacos
Retículo Sarcoplasmático/ultraestrutura
Benzodiazepinas/toxicidade
Coração Fetal/ultraestrutura
Limites: Animais
Gravidez
Camundongos
Responsável: CL61.1 - Biblioteca Central Campus Sur


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Id: lil-742239
Autor: Figueiras, Maria João; Maroco, João; Monteiro, Rita; Caeiro, Raul.
Título: Cardiac misconceptions among healthy adults: implications for the promotion of health in the community / Crenças erróneas sobre as doenças cardíacas em adultos saudáveis: implicações para a promoção da saúde na comunidade
Fonte: Ciênc. saúde coletiva;20(3):841-850, 03/2015. tab, graf.
Idioma: en.
Projeto: Fundação para a Ciência e Tecnologia.
Resumo: This study sought to confirm the structure and to investigate the psychometric properties of an experimental Portuguese version of the York Cardiac Beliefs Questionnaire (YCBQ) in a general population sample. It also set out to identify the prevalent misconceptions in the community and to assess the differences according to socio-demographic characteristics. It involved a cross-sectional survey in which both test and validation samples were collected (n = 476), including participants aged between 18 and 40, recruited via e-mail and social networks. The Confirmatory Factor Analysis on both samples suggested a shorter, three factor version of the YCBQ. Also, misconceptions differed significantly according to sociodemographic variables. The validation of the YCBQ for samples in the community constitutes an important starting point to promote research on misconceptions held in the community by specific groups, as well as to provide key points for health promotion.

Este estudo teve como objetivo confirmar a estrutura e investigar as propriedades psicométricas de uma versão experimental portuguesa do York Cardiac Beliefs Questionnaire numa amostra da população geral; identificar as crenças erróneas mais fortes na comunidade; e avaliar as diferenças de acordo com características sociodemográficas. Trata-se de um estudo transversal com uma amostra de teste e outra de validação, incluindo um total de 476 participantes, com idade entre 18 e 40 anos, recrutados via e-mail e nas redes sociais. A Análise Fatorial Confirmatória em ambas as amostras indicou uma versão reduzida do YCBQ de três factores. As crenças erróneas diferiram significativamente de acordo com as variáveis sociodemográficas. A validação do YCBQ para amostras da comunidade constitui um importante ponto de partida para promover a investigação sobre crenças erróneas em grupos específicos da comunidade, assim como fornecer indicadores relevantes para a promoção da saúde.
Descritores: Cálcio/metabolismo
Inflamação/metabolismo
/metabolismo
INTERLEUKIN-1ABATTOIRS/metabolismo
Proteínas de Membrana/metabolismo
Músculo Liso/metabolismo
Proteínas de Neoplasias/metabolismo
Sistema Respiratório/embriologia
Fator de Necrose Tumoral alfa/metabolismo
-Sítios de Ligação
Células Cultivadas
Canais de Cálcio/metabolismo
Membrana Celular/metabolismo
Miócitos de Músculo Liso/metabolismo
Retículo Sarcoplasmático/metabolismo
Limites: Humanos
Tipo de Publ: Research Support, N.I.H., Extramural
Responsável: BR1.1 - BIREME


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Id: lil-662144
Autor: Roldán Palomo, Ana Rocío; Martín, Pedro; Rebolledo, Alejandro; Enrique, Nicolás; Flores, Luis E.; Milesi, Verónica.
Título: Human umbilical artery smooth muscle exhibits a 2-APB-sensitive capacitative contractile response evoked by vasoactive substances and expresses mRNAs for STIM, Orai and TRPC channels
Fonte: Biocell;36(2):73-81, Aug. 2012. graf, tab.
Idioma: en.
Projeto: Consejo Nacional de Investigaciones Científicas y Técnicas (CONICET). PIP 0202.
Resumo: After depletion of intracellular Ca2+ stores the capacitative response triggers an extracellular Ca2+ influx through store-operated channels (SOCs) which refills these stores. Our objective was to explore if human umbilical artery smooth muscle presented this response and if it was involved in the mechanism of serotonin- and histamine-induced contractions. Intracellular Ca2+ depletion by a Ca2+-free extracellular solution followed by Ca2+ readdition produced a contraction in artery rings which was inhibited by the blocker of Orai and TRPC channels 2-aminoethoxydiphenyl borate (2-APB), suggesting a capacitative response. In presence of 2-APB the magnitude of a second paired contraction by serotonin or histamine was significantly less than a first one, likely because 2-APB inhibited store refilling by capacitative Ca2+ entry. 2-APB inhibition of sarcoplasmic reticulum Ca2+ release was excluded because this blocker did not affect serotonin force development in a Ca2+-free solution. The PCR technique showed the presence of mRNAs for STIM proteins (1 and 2), for Orai proteins (1, 2 and 3) and for TRPC channels (subtypes 1, 3, 4 and 6) in the smooth muscle of the human umbilical artery. Hence, this artery presents a capacitative contractile response triggered by stimulation with physiological vasoconstrictors and expresses mRNAs for proteins and channels previously identified as SOCs.
Descritores: Compostos de Boro/farmacologia
Contração Muscular/efeitos dos fármacos
Músculo Liso/efeitos dos fármacos
Músculo Liso/metabolismo
RNA Mensageiro/genética
Artérias Umbilicais/efeitos dos fármacos
Capacitância Vascular/efeitos dos fármacos
-Western Blotting
Células Cultivadas
Bloqueadores dos Canais de Cálcio/farmacologia
Canais de Cálcio/química
Canais de Cálcio/genética
Canais de Cálcio/metabolismo
Cálcio/metabolismo
Agonistas dos Receptores Histamínicos/farmacologia
Histamina/farmacologia
Proteínas de Membrana/genética
Proteínas de Membrana/metabolismo
Músculo Liso/citologia
Proteínas de Neoplasias/genética
Proteínas de Neoplasias/metabolismo
Reação em Cadeia da Polimerase em Tempo Real
Reação em Cadeia da Polimerase Via Transcriptase Reversa
Retículo Sarcoplasmático/efeitos dos fármacos
Retículo Sarcoplasmático/metabolismo
Agonistas do Receptor de Serotonina/farmacologia
Serotonina/farmacologia
Canais de Cátion TRPC/genética
Canais de Cátion TRPC/metabolismo
Artérias Umbilicais/citologia
Artérias Umbilicais/metabolismo
Limites: Humanos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: AR1.2 - Instituto de Investigaciónes Epidemiológicas


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Id: lil-568135
Autor: Reyes-Juárez, José Luis; Zarain-Herzberg, Ángel.
Título: Función del retículo sarcoplásmico y su papel en las enfermedades cardíacas / Function and role of the sarcoplasmic reticulum in heart disease
Fonte: Arch. cardiol. Méx;76(supl.4):S18-S32, oct.-dic. 2006.
Idioma: es.
Resumo: The sarcoplasmic reticulum (SR) constitutes the main intracellular calcium store in striated muscle and plays an important role in the regulation of excitation-contraction-coupling (ECC) and of intracellular calcium concentrations during contraction and relaxation. The regulation of ECC occurs due to the interaction among the main proteins of the SR that are the calcium release channel or ryanodine receptor, the Ca2+-ATPase, phospholamban and calsequestrin. Due to the importance of ECC in the physiopathology of a number of cardiac diseases, the role of the SR and its components has been widely investigated in some pathologies, specifically cardiac hypertrophy, heart failure, and hereditary arrhythmias. Therefore, the SR proteins constitute an area of research of great interest for the development of new genetic and pharmacologic therapies; from this derives the importance of understanding the function of the SR. This review analyzes the expression, structure, and function of the main SR proteins, their role on myocardial contraction and relaxation and in the changes that occur in cardiac pathologies.
Descritores: Cardiopatias
Contração Miocárdica/fisiologia
Retículo Sarcoplasmático/fisiologia
-Arritmias Cardíacas
Arritmias Cardíacas
Canais de Cálcio
Proteínas de Ligação ao Cálcio
ATPases Transportadoras de Cálcio
Cálcio
Calsequestrina
Cardiomegalia
Cardiomegalia
Cardiopatias
Insuficiência Cardíaca
Insuficiência Cardíaca
Miocárdio
Pesquisa
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático
Retículo Sarcoplasmático
Limites: Humanos
Tipo de Publ: Estudo Comparativo
Revisão
Responsável: BR1.1 - BIREME


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Id: lil-511092
Autor: Fonseca, Silvia Carolina Guatomosim; Stefanon, Ivanita.
Título: Aspectos moleculares do acoplamento excitação-contração na insulficiência cardíaca / Aspectos of molecular compling excitement-contraction in heart failure
Fonte: In: Krieger, José Eduardo. Bases moleculares das Doenças Cardiovasculares: a integração entre a pesquisa e a prática clínica. São Paulo, Atheneu, 2008. p.253-257.
Idioma: pt.
Descritores: Insuficiência Cardíaca
Miócitos Cardíacos/imunologia
-Proteínas Sensoras de Cálcio Intracelular
Retículo Sarcoplasmático
Limites: Humanos
Tipo de Publ: Livro-Texto
Responsável: BR44.1 - Serviço de Biblioteca, Documentação Científica e Didática Prof. Dr. Luiz Venere Décourt


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Id: lil-485645
Autor: Sánchez, Gina; Macho, Pilar; Parra, Víctor; Donoso, Paulina; Domenech, Raúl.
Título: Participación de Ca2+ en el precondicionamiento del miocardio por ejercicio / Role of Ca2+ in exercise induced myocardial preconditioning
Fonte: Rev. chil. cardiol;25(1):85-91, ene.-mar. 2006. ilus, tab.
Idioma: es.
Projeto: FONDECYT; . FONDAP.
Resumo: Antecedentes: Episodios breves de ejercicio previos a la oclusión prolongada de una arteria coronaria disminuyen el tamaño del infarto inducido por ésta. Objetivo: Dado que la administración intracoronaria de Ca2+ induce precondicionamiento, y el ejercicio probablemente aumenta el calcio citosólico, decidimos estudiar si el precondicionamiento por ejercicio está mediado por Ca2+. Material y método: Para ello analizamos el efecto del bloqueo de los canales de calcio del sarcolema, con verapamilo, sobre la acción precondicionante del ejercicio. Se midió tamaño del infarto en perros entrenados a correr en cinta sin finasignados aleatoriamente a los siguientes grupos. I: Isquemia inducida por oclusión coronaria durante 1 hora seguida de reperfusión por 4 hrs. E+I: Similar al grupo I, pero los perros hicieron ejercicio antes de inducir la isquemia. V+I: Similar al grupo I, pero se administró verapamilo antes de inducir la isquemia. V+E+I : Similar al grupo E+I, pero se administró verapamilo antes del ejercicio. Para estudiar el posible rol mediador del retículo sarcoplasmático (RS) en los efectos de la isquemia y de verapamilo, se midió la captación y la liberación de calcio en vesículas de RS de la pared del ventrículo izquierdo sometida a isquemia con o sin verapamilo en perros con y sin precondicionamiento con ejercicio. Los resultados, expresados como promedio +/- ES, se analizaron mediante ANOVA seguido del test de Holm para comparaciones múltiples. Resultados: Verapamilo revirtió el efecto protector del ejercicio sobre el tamaño del infarto (E+I: 6,0 +/- 9,4; N=12 vs V+E+I: 27,7+/-9,6; N=15; P<0.05), pero no modificó el efecto protector del ejercicio precondicionante sobre los trastornos de transporte de calcio en el RS inducidos por la isquemia. Conclusiones: Nuestros resultados sugieren que el precondicionamiento inducido por ejercicio está mediado por la entrada de calcio a la célula...

Background: Brief episodes of exercise prior to a prolonged occlusion of a coronary artery substantially reduce infarct size. Aim: Since the intracoronary administration of Ca2+ induces preconditioning and exercise most likely increases cytosolic calcium we put forward the hypothesis that preconditioning by exercise is mediated by calcium. Methods: For this purpose we analyzed the effect of verapamil, a sarcolemmal calcium channel blocker, on preconditioning by exercise. We measured infarct size in dogs randomly assigned to one of the following groups. I: Ischemia induced by coronary occlusion during 1 hour followed by reperfusion during 4 hours. E+I: Similar to group I, but the dogs run on a treadmill prior to ischemia. V+I: Similar to group I but verapamil was administered before the coronary occlusion. V+E+I: Similar to group E+I but verapamil was administered before exercise. SR vesicles from ventricular tissue were isolated from dogs subjected to the same experimental protocols and calcium release and active calcium uptake were measured. Results were expressed as Mean +/- SE and analyzed by ANOVA followed by Holm test for multiple comparisons. Results: Verapamil reverted the protective effect of exercise on infarct size (E+I: 6,0 +/- 9,4; N=12 vs V+E+I: 27,7 +/- 9,6;N=15; P<0.05) however it did not modify the protective effect of exercise on the alterations produced by ischemia on calcium transport in the RS. Conclusions: These results suggest that the preconditioning effect of exercise is mediated by calcium entering the cell through the sarcolemma but not by exercise effects on SR calcium transport.
Descritores: Cálcio/metabolismo
Infarto do Miocárdio/metabolismo
Isquemia/metabolismo
Precondicionamento Isquêmico Miocárdico
Verapamil/farmacologia
-Análise de Variância
Bloqueadores dos Canais de Cálcio/farmacologia
Grupos Controle
Cães
Infarto do Miocárdio/fisiopatologia
Teste de Esforço/métodos
Retículo Sarcoplasmático/metabolismo
Sarcolema
Sarcolema/metabolismo
Limites: Animais
Responsável: CL1.1 - Biblioteca Central


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Id: lil-461368
Autor: Carreira, A. C. O; Bastos, C. M. V; Verjovski-Almeida, S.
Título: Probing the SERCA1a sarcoplasmic reticulum Ca2+-ATPase phosphorylation-site mutant D351E with inorganic phosphate
Fonte: Braz. j. med. biol. res = Rev. bras. pesqui. méd. biol;40(10):1323-1332, Oct. 2007. ilus.
Idioma: en.
Resumo: The expression of sarcoplasmic reticulum SERCA1a Ca2+-ATPase wild-type and D351E mutants was optimized in yeast under the control of a galactose promoter. Fully active wild-type enzyme was recovered in yeast microsomal membrane fractions in sufficient amounts to permit a rapid and practical assay of ATP hydrolysis and phosphoenzyme formation from ATP or Pi. Mutant and wild-type Ca2+-ATPase were assayed for phosphorylation by Pi under conditions that are known to facilitate this reaction in the wild-type enzyme, including pH 6.0 or 7.0 at 25°C in the presence of dimethylsulfoxide. Although glutamyl (E) and aspartyl (D) residue side chains differ by only one methylene group, no phosphoenzyme could be detected in the D351E mutant, even upon the addition of 40 percent dimethylsulfoxide and 1 mM 32Pi in the presence of 10 mM EGTA and 5 mM MgCl2. These results show that in the D351E mutant, increasing hydrophobicity of the site with inorganic solvent was not a sufficient factor for the required abstraction of water in the reaction of E351 with Pi to form a glutamylphosphate (P-E351) phosphoenzyme moiety. Mutation D351E may disrupt the proposed alignment of the reactive water molecule with the aspartylphosphate (P-D351) moiety in the phosphorylation site, which may be an essential alignment both in the forward reaction (hydrolysis of aspartylphosphate) and in the reverse reaction (abstraction of water upon formation of an aspartylphosphate intermediate).
Descritores: Mutação/genética
Fosfatos/metabolismo
Saccharomyces cerevisiae/genética
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/genética
Retículo Sarcoplasmático/enzimologia
-Regulação Fúngica da Expressão Gênica
Vetores Genéticos
Fosforilação
Saccharomyces cerevisiae/metabolismo
ATPases Transportadoras de Cálcio do Retículo Sarcoplasmático/metabolismo
Limites: Animais
Coelhos
Tipo de Publ: Research Support, Non-U.S. Gov't
Responsável: BR1.1 - BIREME


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Id: lil-443671
Autor: Hidalgo, C; Bull, R; Marengo, J. J; Perez, C. F; Donoso, P.
Título: SH oxidation stimulates calcium release channels (ryanodine receptors) from excitable cells
Fonte: Biol. Res;33(2):113-124, 2000. graf.
Idioma: en.
Projeto: Fondo Nacional de Investigación Científica y Tecnológica.
Resumo: The effects of redox reagents on the activity of the intracellular calcium release channels (ryanodine receptors) of skeletal and cardiac muscle, or brain cortex neurons, was examined. In lipid bilayer experiments, oxidizing agents (2,2'-dithiodipyridine or thimerosal) modified the calcium dependence of all single channels studied. After controlled oxidation channels became active at sub microM calcium concentrations and were not inhibited by increasing the calcium concentration to 0.5 mM. Subsequent reduction reversed these effects. Channels purified from amphibian skeletal muscle exhibited the same behavior, indicating that the SH groups responsible for modifying the calcium dependence belong to the channel protein. Parallel experiments that measured calcium release through these channels in sarcoplasmic reticulum vesicles showed that following oxidation, the channels were no longer inhibited by sub mM concentrations of Mg2+. It is proposed that channel redox state controls the high affinity sites responsible for calcium activation as well as the low affinity sites involved in Mg2+ inhibition of channel activity. The possible physiological and pathological implications of these results are discussed.
Descritores: Canal de Liberação de Cálcio do Receptor de Rianodina/efeitos dos fármacos
Compostos de Sulfidrila/farmacologia
Córtex Cerebral/citologia
Miócitos Cardíacos/metabolismo
Neurônios/metabolismo
Retículo Sarcoplasmático/metabolismo
-Anuros
Canal de Liberação de Cálcio do Receptor de Rianodina/metabolismo
Oxirredução
Limites: Animais
Coelhos
Ratos
Responsável: BR1.1 - BIREME


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Id: lil-437517
Autor: Matthew, A; Shmygol, A; Wray, Susan.
Título: Ca2+ entry, efflux and release in smooth muscle
Fonte: Biol. Res;37(4):617-624, 2004. graf.
Idioma: en.
Resumo: Control of smooth muscle is vital for health. The major route to contraction is a rise in intracellular [Ca2+], determined by the entry and efflux of Ca2+ and release and re-uptake into the sarcoplasmic reticulum (SR). We review these processes in myometrium, to better understand excitation-contraction coupling and develop strategies for preventing problematic labours. The main mechanism of elevating [Ca2+] is voltage-gated L-type channels, due to pacemaker activity, which can be modulated by agonists. The rise of [Ca2+] produces Ca-calmodulin and activates MLCK. This phosphorylates myosin and force results. Without Ca2+ entry uterine contraction fails. The Na/Ca exchanger (NCX) and plasma membrane Ca-ATPase (PMCA) remove Ca2+, with contributions of 30 percet and 70 percet respectively. Studies with PMCA-4 knockout mice show that it contributes to reducing [Ca2+] and relaxation. The SR contributes to relaxation by vectorially releasing Ca2+ to the efflux pathways, and thereby increasing their rates. Agonists binding produces IP3 which can release Ca from the SR but inhibition of SR Ca2+ release increases contractions and Ca2+ transients. It is suggested that SR Ca2+ targets K+ channels on the surface membrane and thereby feedback to inhibit excitability and contraction.
Descritores: /fisiologia
ATPASA TRANSPORTADORA DE CA(TEMEFOS+)/fisiologia
/metabolismo
ATPASA TRANSPORTADORA DE CA(TEMEFOS+)/metabolismo
Cálcio/metabolismo
Contração Uterina/fisiologia
Contração Uterina/metabolismo
Miométrio/fisiologia
Miométrio/metabolismo
Retículo Sarcoplasmático/fisiologia
Retículo Sarcoplasmático/metabolismo
-Canais de Cálcio Tipo L/metabolismo
Canais de Cálcio/metabolismo
Músculo Liso/fisiologia
Limites: Ratos
Animais
Feminino
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BIREME/OPAS/OMS - Centro Latino-Americano e do Caribe de Informação em Ciências da Saúde