Kallikrein-kininogen-kinin systems are now topics of widespread intere
st. The long-standing appreciation of their diverse pharmacological pr
operties and biochemical characteristics is being supplemented by mode
rn definitions of their cellular receptors' signal-transduction mechan
isms and physiological and pathological roles. The assignment of impor
tant homeostatic responsibilities for kinins, including those in autoc
rine and paracrine signaling for skeletal and cardiac muscle energy me
tabolism, is now subject to definitive experimental evaluation via the
availability of better kallikrein inhibitors, specific kinin receptor
antagonists, and techniques of genetic manipulation.