Kallinergic

Kallinergic is not a widely standardized term in modern medical literature. When it appears, it is often used informally to refer to signaling related to kallikreins or kinins, especially bradykinin and kallidin, rather than to a distinct, established category. Because usage varies and some authors may treat the word as a misspelling or misnomer, researchers and clinicians typically prefer more precise terminology such as kallikrein-kinin system or kinergic signaling.

The kallikrein-kinin system (KKS) is a hormonal cascade that involves kallikreins, kininogens, and kinins. Plasma kallikrein cleaves high-molecular-weight kininogen to release bradykinin, while tissue kallikreins act on kininogens to generate kallidin, which is rapidly converted to bradykinin. Bradykinin and kallidin are short-lived peptide mediators that exert multiple effects on blood vessels and nerves.

Kinins act primarily through two G protein-coupled receptors, B1 and B2. The B2 receptor is constitutively expressed in many tissues and mediates most acute actions such as vasodilation and increased vascular permeability. The B1 receptor is inducible and upregulated during inflammation. Through these receptors, kinins contribute to pain, edema, smooth muscle contraction, and modulation of inflammatory responses.

Clinical and pharmacological relevance is significant. Excessive kallikrein-kinin activity contributes to hereditary angioedema and ACE inhibitor–associated angioedema and cough. Therapeutic approaches include kallikrein inhibitors and bradykinin receptor antagonists, such as those targeting the B2 receptor. In summary, while kallinergic is not a standard term, it is commonly associated with kallikrein-kinin signaling and its physiological and clinical implications.

If encountered, clarify the intended meaning and prefer established terms such as kallikrein-kinin system or kinergic signaling.