High-Glucose Enhances a Thromboxane A_2-Induced Aortic Contraction Mediated by an Alteration of Phosphatidylinositol Turnover
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概要
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The effect of the thromboxane A2 analogue U46619 (9,11-dideoxy-11α,9α-epoxymethanoprostaglandin F2α) on sustained contraction in the mouse aorta was investigated. U46619 induced concentration-dependent (1 – 100 nM) increases in contraction. These contractile responses were enhanced significantly under high-glucose-physiological salt solution (HG-PSS) (2-fold greater than normal-PSS) conditions. This hyperactivation may be associated with aortic dysfunction in diabetes. However, the mechanisms remain unclear. HG-PSS enhanced U46619-induced accumulation of endogenous diacylglycerol (DG). Phospholipase C inhibitor (U73122) suppressed DG accumulation under normal conditions; however, suppression was not observed under high-glucose conditions. The HG-PSS-induced enhancement of contraction was inhibited by protein kinase C (PKC) inhibitor (calphostin C). This result indicated that accumulated DG might increase PKC activity, which then stimulates DG kinase activation as a feedback mechanism. DG kinase inhibition also suppressed HG-PSS-induced enhancement of contraction. Increased myo-inositol incorporation was detected under high-glucose conditions, indicating an acceleration of phosphatidylinositol (PI)-turnover. Moreover, rho kinase inhibitor (Y27632) suppressed U46619-induced contraction exclusively in normal-PSS. These findings indicated that HG-PSS treatment increases DG synthesis derived from incorporated glucose, PKC and DG kinase activation, and enhances the U46619-induced contraction via acceleration of PI-turnover. This series of responses may be involved in the dysfunction of aorta under high-glucose conditions occurring in association with diabetes.
- 社団法人 日本薬理学会の論文
- 2003-07-01
著者
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SUZUKI Hikaru
Department of Physiology, Nagoya City University Medical School
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MOMOSE Kazutaka
Department of Pharmacology, School of Pharmaceutical Sciences, Showa University
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Nobe Koji
Department of Pharmacology, School of Pharmacy, Showa University, Japan
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Sakai Y
Division Of Physiology Department Of Occupational Therapy School Of Nursing And Rehabilitation Scien
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NOBE Hiromi
Department of Phamacology, School of Pharmaceutical Sciences, Showa University
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SAKA Yasushi
Division of Physiology, Department of Occupational Therapy, School of Nursing and Rehabilitation Sci
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Nobe Hiromi
Department Of Phamacology School Of Pharmaceutical Sciences Showa University
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Nobe Koji
Department Of Phamacology School Of Pharmaceutical Sciences Showa University
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Suzuki Hikaru
Department Of Cell Physiology Nagoya City University Medical School
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Suzuki Hikaru
Department Of Phamacology School Of Pharmaceutical Sciences Showa University
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Saka Yasushi
Division Of Physiology Department Of Occupational Therapy School Of Nursing And Rehabilitation Scien
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Momose Kazutaka
Department Of Phamacology School Of Pharmaceutical Sciences Showa University
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Suzuki Hikaru
Department Of Cardiology Tokyo Women's Medical University
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