Kallikrein-kinin system in severe experimental hypertension

Plasma levels of low and high molecular weight kininogens, prokallikrein and active kallikrein were determined in four models of experimental hypertension and in genetically hypertensive rats. The high molecular weight kininogen remained essentially unaltered in all groups, whereas the low molecular weight kininogen was decreased in the renovascular groups. In the glucocorticoid hypertensive rats low molecular weight kininogen increased, but rats with hypertension induced both by renovascular and glucocorticoid mechanisms had normal kininogen. Genetically hypertensive rats had levels of low molecular weight kininogen similar to the ones observed in control group. The data presented reinforce the hypothesis of a participation of the kallikrein-kinin system in the etiopathogenesis of hypertension, indicating an implication of the low molecular weight kininogen in some types of severe experimental hypertension.