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[Interaction between bradykinin and enkephalins in rat dental pulp]
Zhongguo Yao Li Xue Bao = Acta Pharmacologica Sinica
|November 1, 1989
Summary
Bradykinin (BK) and its byproducts activate enkephalin (EK) production in rat dental pulp following cavity formation. This EK then appears to inhibit further BK production, suggesting a regulatory feedback loop.
Area of Science:
- Biochemistry
- Neuroscience
- Dental Research
Context:
- Dental pulp tissue exhibits increased bradykinin (BK)-like peptides after cavity formation.
- Enkephalin (EK)-like peptides are also elevated by cavity formation or BK administration.
- The interplay between BK and EK in dental pulp warrants further investigation.
Purpose:
- To elucidate the mechanism by which BK enhances enkephalin (EK) production in rat dental pulp.
- To investigate the role of specific BK metabolites in EK processing.
- To explore the potential feedback mechanism between EK and BK in the dental pulp.
Summary:
- Bradykinin (BK) and its metabolites, des-Arg9-BK and arginine (Arg), activate benzoyl-L-arginine-2-naphthylamide (BANA)-degrading enzymes, suggesting enhanced processing of enkephalins (EK) from precursor proteins.
- These activating effects on BANA degradation were inhibited by EGTA, indicating a calcium-dependent mechanism.
- Lysosomal enzymes were activated by BK, des-Arg9-BK, and Arg, while soluble enzymes were activated by Arg only.
- Morphine and met-EK inhibited BK production from plasma kininogen, suggesting a negative feedback loop where produced EK reduces BK levels.
Impact:
- This study reveals a novel biochemical pathway regulating pain and inflammation mediators in the dental pulp.
- Understanding this BK-EK interaction may lead to new therapeutic strategies for dental pain and pulpitis.
- The findings highlight the complex neurochemical environment within the dental pulp in response to injury.