Bradykinin – Function, Effects and Clinical Relevance
Bradykinin is an endogenous peptide hormone that regulates inflammation, pain perception, and vasodilation. It plays a central role in the kallikrein-kinin system.
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Bradykinin is an endogenous peptide hormone that regulates inflammation, pain perception, and vasodilation. It plays a central role in the kallikrein-kinin system.
What is Bradykinin?
Bradykinin is a biologically active nine-amino-acid peptide that functions as a key mediator of inflammation, pain, and blood pressure regulation in the human body. It belongs to the group of kinins and is produced as part of the kallikrein-kinin system. The name is derived from the Greek words for slow (bradys) and to move (kinein), referring to the slow contraction of intestinal smooth muscle that bradykinin induces.
Formation and Mechanism of Action
Bradykinin is generated through the enzymatic cleavage of the precursor protein kininogen by the enzyme kallikrein. This reaction can be triggered by various stimuli such as tissue injury, infection, or allergic responses.
Bradykinin exerts its effects through binding to specific receptors:
- B1 receptors: Primarily upregulated during chronic inflammation and involved in persistent pain signaling.
- B2 receptors: Constitutively expressed and responsible for mediating most of the acute effects of bradykinin.
Physiological Effects
Bradykinin is involved in a wide range of physiological and pathophysiological processes:
- Vasodilation: Bradykinin relaxes the smooth muscle of blood vessel walls, leading to a reduction in blood pressure.
- Increased vascular permeability: It increases the leakiness of capillary walls, which can result in tissue swelling (edema).
- Pain induction (nociception): Bradykinin activates pain receptors (nociceptors) in tissue and is one of the most potent endogenous pain mediators.
- Pro-inflammatory signaling: It stimulates the release of additional inflammatory mediators such as prostaglandins and cytokines.
- Bronchoconstriction: In the lungs, bradykinin can trigger narrowing of the airways.
Clinical Relevance
Bradykinin and the Renin-Angiotensin System
Bradykinin is degraded by the enzyme angiotensin-converting enzyme (ACE). ACE inhibitors, which are commonly prescribed for high blood pressure, block this degradation. This leads to an increase in bradykinin levels in the blood, which contributes to their blood-pressure-lowering effect but also explains the characteristic dry cough that is a well-known side effect of ACE inhibitors.
Hereditary Angioedema
Bradykinin plays a particularly important clinical role in hereditary angioedema (HAE). In this rare genetic condition, uncontrolled bradykinin release causes potentially life-threatening swelling of the skin, mucous membranes, and internal organs. Specific bradykinin antagonists such as icatibant are used to treat acute attacks of this condition.
Pain and Inflammation
Because bradykinin is a potent pain-inducing mediator, it is the subject of intensive research into new analgesic drugs. Bradykinin receptor antagonists may play a future role in the management of chronic pain conditions.
Degradation of Bradykinin
Bradykinin has a very short half-life in the bloodstream of only a few seconds. It is primarily broken down by the following enzymes:
- ACE (angiotensin-converting enzyme)
- Neutral endopeptidase (neprilysin)
- Aminopeptidase P
- Carboxypeptidase N
This rapid degradation limits the local and systemic effects of bradykinin under normal physiological conditions.
References
- Kaplan, A.P. & Ghebrehiwet, B. (2010): The plasma bradykinin-forming pathways and its interrelationships with complement. Molecular Immunology, 47(13), 2161-2169.
- Rhaleb, N.E. et al. (2011): The kallikrein-kinin system as a regulator of cardiovascular and renal function. Comprehensive Physiology, 1(2), 971-993.
- Cicardi, M. et al. (2014): Evidence-based recommendations for the therapeutic management of angioedema owing to hereditary C1 inhibitor deficiency. Allergy, 69(5), 602-616.
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