Bradykininmediärt

Bradykininmediärt refers to physiological and pathophysiological processes that are mediated by bradykinin, a nonapeptide in the kallikrein–kinin system. Bradykinin is generated from kininogen by plasma kallikrein during inflammatory and coagulation responses. It exerts its effects primarily via the bradykinin B2 receptor, while des-Arg-bradykinin acts mainly on the B1 receptor, especially in inflamed tissues.

Key effects include rapid vasodilation and increased vascular permeability, leading to edema. Bradykinin also sensitizes nociceptors, contributing to pain, and stimulates the release of mediators such as nitric oxide and prostacyclin from endothelial cells. In normal physiology these processes support tissue perfusion and immune responses; in pathology, excessive bradykinin activity can contribute to edema and cough.

Clinical relevance is exemplified by conditions such as hereditary angioedema, which can result from C1 esterase inhibitor deficiency and leads to uncontrolled bradykinin production. Medications that alter bradykinin levels, notably angiotensin-converting enzyme inhibitors, can cause bradykinin-mediated cough and angioedema. Therapeutic approaches to bradykinin-mediated angioedema include bradykinin B2 receptor antagonists (for example icatibant) and kallikrein inhibitors (such as ecallantide or newer agents) to reduce bradykinin generation or action.

Bradykininmediärt mechanisms intersect with the broader inflammatory response and the contact system, representing a distinct pathway from histamine-mediated vascular effects but with overlapping clinical manifestations in edema and pain.