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Dexmedetomidine-Induced Aortic Contraction Involves Transactivation of the Epidermal Growth Factor Receptor in Rats
Soo Hee Lee1,2,3, Seong-Chun Kwon4, Seong-Ho Ok1,2,3
1Department of Anesthesiology and Pain Medicine, Gyeongsang National University Changwon Hospital 11, Samjeongja-ro, Seongsan-gu, Changwon-si 51472, Gyeongsangnam-do, Korea.
International Journal of Molecular Sciences
|April 23, 2022
Summary
Dexmedetomidine-induced aortic contraction involves epidermal growth factor receptor (EGFR) transactivation. This process is mediated by alpha-2 adrenoceptors, Src kinase, and matrix metalloproteinases, leading to JNK phosphorylation and increased calcium levels.
Area of Science:
- Pharmacology
- Cardiovascular Physiology
- Molecular Biology
Background:
- Alpha-2 adrenoceptor agonists like dexmedetomidine can induce aortic contraction.
- The role of epidermal growth factor receptor (EGFR) transactivation in this process is not fully understood.
Purpose of the Study:
- To investigate the involvement of EGFR transactivation in dexmedetomidine-induced aortic contraction.
- To elucidate the underlying cellular mechanisms, including the roles of Src kinase and matrix metalloproteinases.
Main Methods:
- Isolated endothelium-denuded rat aortas were used to study aortic contraction.
- The effects of various inhibitors (rauwolscine, AG1478, PP1, PP2, GM6001, prazosin) on dexmedetomidine-induced effects were examined.
- EGFR and JNK phosphorylation were assessed, along with the impact of EGFR siRNA.
Main Results:
- Dexmedetomidine-induced aortic contraction was inhibited by alpha-2 adrenoceptor antagonists, EGFR inhibitors, Src kinase inhibitors, and matrix metalloproteinase inhibitors.
- EGFR and JNK phosphorylation induced by dexmedetomidine were similarly inhibited by these agents.
- EGFR siRNA treatment reduced dexmedetomidine-induced JNK phosphorylation.
Conclusions:
- EGFR transactivation is implicated in dexmedetomidine-induced aortic contraction.
- The alpha-2 adrenoceptor, Src kinase, and matrix metalloproteinases mediate this EGFR transactivation, leading to JNK phosphorylation and elevated calcium levels.
