Bradykinin modulates ion channel in inflammatory pain.
- Author:
Bo-Yi LIU
1
;
Hai-Lin ZHANG
Author Information
1. Department of Pharmacology, School of Basic Medicine, Hebei Medical University, Shijiazhuang 050017, China.
- Publication Type:Journal Article
- MeSH:
Acid Sensing Ion Channels;
Animals;
Bradykinin;
pharmacology;
physiology;
Humans;
Inflammation;
complications;
Inflammation Mediators;
pharmacology;
physiology;
Ion Channels;
KCNQ Potassium Channels;
metabolism;
physiology;
Nerve Tissue Proteins;
metabolism;
Pain;
etiology;
metabolism;
physiopathology;
Receptors, AMPA;
metabolism;
Receptors, N-Methyl-D-Aspartate;
metabolism;
Receptors, Purinergic P2X3;
metabolism;
Sodium Channels;
metabolism;
TRPA1 Cation Channel;
TRPV Cation Channels;
metabolism;
physiology;
Transient Receptor Potential Channels;
metabolism;
physiology
- From:
Acta Pharmaceutica Sinica
2009;44(10):1066-1071
- CountryChina
- Language:Chinese
-
Abstract:
Injury or inflammation induces release of a range of inflammatory mediators. Bradykinin is one of the most important inflammatory mediators and plays a crucial role in mediating inflammatory pain. It is well known that multiple ion channels located in the nociceptors participate in pain sensation. Recent studies demonstrate an important role of bradykinin in regulating the function and expression of pain-related ion channels. This paper summarizes the recent advances in the understanding of the role of bradykinin in modulation of the channels and discusses future possibilities in the treatment of inflammatory pain.
