Consumo de cininogênio plasmático humano 'in vitro', causado por catecolaminas

• Ano de defesa: 1983
• Autor(a) principal: Assreuy Filho, Jamil
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Palavras-chave em Português: Cininogênio de Alto Peso Molecular; Farmacologia; Catecolaminas
• Link de acesso: http://www.repositorio.ufc.br/handle/riufc/65891

The present work have shown that human blood kininogen obtained from normal donors was partially reduced by adrenaline and noradrenaline. Isopropyl- noradrenaline was ineffective in this way. This effect of catecholamines seemed to be dosedependent and required the presence of leukocytes, since kininogen of cell-free plasma was not reduced after exposure to catecholamones. Esterolytic activity towards benzoyl-arginine-ethyl-ester (BAEe) was gene- rated by incubation of leukocyte-rich plasma with adrenaline. On the other hand, incubation of leukocytes with adrenaline have failed to evoke this este— rolytic activity when plasma was substituted by Hank’s. The kininogen-reducing activity showed by adrenaline and noradrenaline was inhibited by phenoxy- benzamine, aspirin and soy bean trypsin inhibitor (SBTI) and was unaffected by indomethacin. The amount of bradykinin potentiating factors derived from adre- naline-treated blood was not different from those derived from control blood. Tnese results led us to the following con- clusions: a The effect of catecholamines appeared to be -adrenergic. b) The consumption of plasma kininogen was a real fenomenum and could not be attributable to a re- duced amount of bradykinin potentiating factors. c) The presence of leukocytes was an absolu- te pre-requisite for the catecholamine-mediated kininogen consumption. d) The inhibitory effect of aspirin may be acting in other systems besides prostaglandin-synthe - tase. e) Probably the main adrenaline-activated esterase was plasma kallikrein.