The physiological and pathological effects of the nonapeptide bradykin
in (BK) are mediated via the activation of at least two types of brady
kinin receptors termed B1 and B2. The B2 type is the most prevalent un
der physiological conditions and is preferentially activated by BK. Th
e B1 type is selectively activated by des-Arg9-BK and seems to be grea
tly induced in some pathological states. Both B1 and B2 bradykinin rec
eptors have had their cDNAs cloned and belong to the seven transmembra
ne coupled G-protein receptor family. BK receptor activation stimulate
s the transduction pathways leading to the generation of different sec
ond messengers (Ca2+, prostaglandins, NO, cGMP). It is suggested that
bradykinin receptors are involved in various different physiological a
nd physiopathological mechanisms such as the control of blood pressure
and cardiovascular functions, the inflammatory reaction (allergy, ast
hma, oedema). Therefore it appears that bradykinin receptors activatio
n can be involved in beneficial and deleterious effects and thus the d
evelopment of both long lasting agonists and antagonists are of therap
eutical interest.