Consumption of kininogen, formation of kinin and activation of arginine ester hydrolase in rat plasma by rat peritoneal fluid cells in the presence of l-adrenaline

Abstract

Cells harvested from the peritoneal cavity of the rat, were able to lower kininogen, release kinin and activate benzoylarginine ester (BAEE) hydrolase following brief incubation with rat plasma in the presence of l-adrenaline. These effects were not reproduced when either cells or the catecholamine were incubated with plasma. Peritoneal cells incubated with l-adrenaline did not acquire detectable BAEE-esterase activity, but became able to induce this activity as well as lowering of kininogen, in adrenaline-free plasma. Phenoxybenzamine and, to a lesser extent, propranolol, blocked the action of adrenaline, which was also sensitive to Trasylol, the anti-kallikrein inhibitor from bovine tissues. l-Noradrenaline was less effective than adrenaline, isoprenaline, ineffective. Peritoneal cavity washings which contained no mast cells, but were normal in their lymphocyte and eosinophil content, were unable to lower plasma kininogen in the presence of l-adrenaline. Pretreatment with compound 48/80, leading to substantial release of histami did not decrease the cells' ability to lower plasma kininogen in the presence of adrenaline. The catecholamine failed to release histamine from peritoneal fluid cells. Acetylsalicylic acid (Aspirin®) blocked cell-linked lowering of kininogen and the activation of BAEE-esterase by l-adrenaline. This effect was obtained at a dose (2–10 μg/ml) of the analgesic, 200–500 times lower than that required to block histamine release by compound 48/80. While the action of acetylsalicyclic acid on this release was counteracted by glucose, its effect on kininogen breakdown and esterase activation occurred in the presence of physiological levels of the sugar. While peritoneal fluid cells pretreated with acetylsalicylic acid could not be activated by adrenaline, the action of adrenaline-activated cells on plasma kininogen and BAEE-esterase was not inhibited by the presence of acetylsalicylic acid in the incubation medium. Acetylsalicylic acid prevented the appearance of the discrete morphological alterations normally evoked by adrenaline in rat mesentery mast cells, but failed to affect the degranulation evoked in these cells by compound 48/80.