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

Abstract

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.