The Mechanism of Bradykinin Edema

Abstract

It is well established that bradykinin, administered locally, increases the efflux rate of water from capillaries and venules in systemic vascular beds. The mechanism of this effect, however, is not so well established. The major question yet to be answered is whether it results from: 1.) a direct action on the membrane, 2.) indirectly from actions on vascular smooth muscle, or 3.) both. Does bradykinin increase the rate of water efflux by directly increasing the permeability of the capillary and venular wall to protein, thereby reducing effective colloid asmotic pressure, or does it first act on the muscle in arteries, arteriovenous anastomosis, and veins in such a manner as to cause a rise in effective capillary hydrostatic pressure? Both actions could account for the edema, as well as for the repeatedly observed increased efflux rate of protein. It is the purpose of this paper to review studies from our laboratory in the dog forelimb, hind-limb and lung bearing on these questions. The studies suggest that more attention should be given the possibility that a rise in effective capillary hydrostatic pressure is importantly involved in the production of the edema.