Properties of acetylcholine-induced hyperpolarization in smooth muscle cells of the mouse mesenteric artery
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概要
- 論文の詳細を見る
The properties of smooth muscle cell hyperpolarization produced by acetylcholine (ACh) were investigated in mesenteric arteries isolated from mice. The resting membrane potential of the smooth muscle cells was about -60mV. When ACh (10μM) was applied for 1min, the membrane hyperpolarized with a peak amplitude of about 5 mV which was reached in about 1 min, following which the potential slowly reverted to the resting level over about 7 min following withdrawal of ACh from the superfusate (recovery component). Exposure of the artery to 0.5 mM Ba^<2+>, an inhibitor of inward rectifier K-channels, depolarized the membrane by about 13 mV, increased the amplitude of the ACh-induced hyperpolarization to about 10 mV, and facilitated the visualization of the recovery component. Indomethacine (10μM), an inhibitor of cyclooxygenase, inhibited the recovery component and as a consequence reduced the duration of the hyperpolarization. The ACh-induced response was not markedly altered by either N^ω-nitro-L-arginine (10μM), an inhibitor of nitric oxide (NO) production, or catalase (130 U/ml), a super oxide scavenger. Exogenously applied hydrogen peroxide (H_2O_2, 300μM) hyperpolarized the membrane by about 5 mV, which was abolished by catalase. These results suggest that in the mouse mesenteric artery, the ACh-induced hyperpolarization has two components, both an indomethacin-sensitive and an indomethacin-insensitive component. The former component may be produced by prostanoids, while the latter may be produced by factors other than NO or H_2O_2. The results also suggested that the inward rectifier K-channels may be important for producing the resting membrane potential, but they may not be the main contributor to the ACh-induced hyperpolarization of smooth muscle cell membranes in the mouse mesenteric artery.
- 日本平滑筋学会の論文
著者
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Yokoyama Y
Department Of Physiology Nagoya City University School Of Nursing
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Yokoyama Yoshifumi
First Department Of Internal Medicine Nagoya City University School Of Medicine
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Ueno Hikaru
Department of Public Health, Tokai University School of Medicine
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Yamamoto Y
Department Of Physiology Nagoya City University School Of Nursing
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KOSHITA Makoto
Department of Physiology, Nagoya City University Medical School
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HIDAKA Kiyoshi
Department of Biochemistry and Molecular Pathophysiology, Faculty of Medicine, University of Occupat
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YAMAMOTO Yoshimichi
Department of Physiology, Nagoya City University School of Nursing
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SUZUKI Hikaru
Department of Physiology, Nagoya City University Medical School
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Ueno Hikaru
Department Of Biochemistry And Molecular Pathophysiology Faculty Of Medicine University Of Occupatio
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Yokoyama Yoshifumi
The First Department Of Internal Medicine Nagoya City University Medical School
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Suzuki H
Department Of Physiology Nagoya City University Medical School
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Suzuki Hikaru
Department Of Physiology Nagoya City University Medical School
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Suzuki Hikaru
Department Of Cell Physiology Nagoya City University Medical School
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Yamamoto Yoshimichi
Laboratory Of Physiology Nagoya City University School Of Nursing
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Yamamoto Y
Department Of Physiology Nagoya City University Nursing School
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Yamamoto Yoshimichi
Department Of Civil Engineering
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Hidaka Kiyoshi
Department Of Biochemistry And Molecular Pathophysiology Faculty Of Medicine University Of Occupatio
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Suzuki Hikaru
Dep. Of Cell Physiology
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Koshita M
Department Of Physiology Nagoya City University Medical School
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Yamamoto Yoshimichi
Lab. Of Physiology Nagoya City Univ. School Of Nursing
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Suzuki Hikaru
Department Of Cardiology Tokyo Women's Medical University
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Koshita Makoto
Department of Cell Physiology, Graduate School of Medical Sciences, Nagoya City University
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