Controversial Effect of Ethanol Irrespective of Kinases Inhibition on the Agonist-Dependant Vasoconstriction
- Authors
- Je, Hyun Dong; Kim, Hyeong-Dong; Park, June Hong
- Issue Date
- 31-5월-2012
- Publisher
- KOREAN SOC APPLIED PHARMACOLOGY
- Keywords
- Ethanol; Phorbol ester; Rho-kinase; Thromboxane A(2) mimetic; Vasodilation
- Citation
- BIOMOLECULES & THERAPEUTICS, v.20, no.3, pp.352 - 356
- Indexed
- SCIE
SCOPUS
KCI
- Journal Title
- BIOMOLECULES & THERAPEUTICS
- Volume
- 20
- Number
- 3
- Start Page
- 352
- End Page
- 356
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/108389
- DOI
- 10.4062/biomolther.2012.20.3.352
- ISSN
- 1976-9148
- Abstract
- The present study was undertaken to determine whether ethanol influences on the agonist-induced vascular smooth muscle contraction and, if so, to investigate the related mechanism. The measurement of isometric contractions using a computerized data acquisition system was combined with molecular experiments. Ethanol significantly inhibited thromboxane A(2) mimetic-induced contraction with intact endothelial function, but there was no relaxation on thromboxane A(2) mimetic U-46619-induced contraction irrespective of endothelium suggesting that the pathway such as Rho-kinase activation, Ca2+ entry or thin filament regulation was not affected. In addition, ethanol didn't decrease thromboxane A(2) mimetic-induced increase of phospho-myosin phosphatase targeting subunit protein 1 (pMYPT1) or pERK1/2. Interestingly, ethanol didn't inhibit significantly phorbol ester-induced contraction in denuded muscles suggesting that thin filament regulation is less important on the ethanol-induced regulation in the muscle than endothelial NO synthesis. In conclusion, this study provides the evidence and possible related mechanism concerning the effect of ethanol on the agonist-dependent contraction in rat aortic rings with regard to endothelial function.
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