The Kinin‐forming and Kininase Activities of Rabbit Polymorphonuclear Leucocytes*

The major pathway for bradykinin and kallidin formation in the extracellular compart- ments in the body is by cleavage of the blood protein bradykininogen by kallikreins as demonstrated by Werle (1955) and by Pierce & Webster (1961). Inactivation of these peptides is mediated by carboxypeptidases as shown by Erdds & Sloane (1962). Additional reactions leading to kinin formation and destruction have been shown by Greenbaum & Yamafuji (1966, 1966a) to be possibly mediated by tissue cathepsins. Lewis (1963, 1964) has postulated that bradykinin and kallidin may contribute to the signs and pathological responses seen in inflammation since these peptides can cause increased capillary permeability, migration of leucocytes, vasodilatation and pain. The question remains unanswered as to the actual role of these kinins in inflammation- that is, whether they are produced during the inflammatory state. Indeed, Janoff has presented evidence that the inflammatory response may be mediated by agents which are not kinins (Janoff, Bean & Schuller, 1965) but which are basic proteins which have no enzymatic activity.