kallidin

Kallidin, also known as lysyl-bradykinin, is a peptide mediator in the kallikrein–kinin system. It is a decapeptide produced from high-molecular-weight kininogen by kallikrein and serves as an N-terminally extended form of bradykinin. In physiology, kallidin is generated in plasma and various tissues when the contact system is activated, and it can be converted to bradykinin by peptide processing that removes the extra N-terminal lysine.

Kallidin exerts its biological effects primarily through the kallinergic receptors, mainly the B2 receptor, with possible activity at B1 receptors under certain inflammatory conditions. Its actions resemble those of bradykinin and include vasodilation, increased vascular permeability, smooth muscle contraction, and sensitization of pain pathways. These effects are mediated in part by the release of endothelium-derived nitric oxide and prostacyclin, contributing to edema and inflammatory responses.

Metabolism of kallidin occurs rapidly via kininases in plasma and tissues, and it is eventually degraded to inactive metabolites. Through enzymatic processing, kallidin can be shortened to bradykinin, integrating it into the broader kinins system that modulates vascular tone, permeability, and nociception. The overlapping activities of kallidin and bradykinin help explain many inflammatory and cardiovascular responses mediated by the kallikrein–kinin pathway.

Clinical relevance: The kallikrein–kinin system participates in inflammation, pain, and edema. Inhibitors of angiotensin-converting enzyme (ACE) can elevate kinins, contributing to ACE inhibitor–associated cough and angioedema, with both bradykinin and kallidin involved in these processes. Kallidin is one of several kinins that mediate these physiological and pathophysiological effects.