| Item type |
学術雑誌論文 / Journal Article_02(1) |
| 公開日 |
2016-04-04 |
| タイトル |
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|
タイトル |
Endothelin-1, but not angiotensin II, induces afferent arteriolar myosin diphosphorylation as a potential contributor to prolonged vasoconstriction |
| 言語 |
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|
言語 |
eng |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
afferent arteriole |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
angiotensin II |
| キーワード |
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|
主題Scheme |
Other |
|
キーワード |
diphosphorylation |
| キーワード |
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|
主題Scheme |
Other |
|
キーワード |
endothelin-1 |
| キーワード |
|
|
主題Scheme |
Other |
|
キーワード |
myosin regulatory light chain |
| キーワード |
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主題Scheme |
Other |
|
キーワード |
Rho-associated kinase |
| 資源タイプ |
|
|
資源タイプ |
journal article |
| 著者 |
竹谷, 浩介
Xuemei, Wang
Iris, Kathol
Kathy, Loutzenhiser
Rodger, Loutzenhiser
Michael, P. Walsh
|
| 著者 ローマ字 |
|
|
|
Takeya, Kosuke |
| 書誌情報 |
Kidney International
巻 87,
号 2,
p. 370-381,
発行日 2015-02-01
|
| ISSN |
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収録物識別子タイプ |
ISSN |
|
収録物識別子 |
0085-2538 |
| DOI |
|
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関連タイプ |
isVersionOf |
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|
識別子タイプ |
DOI |
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|
関連識別子 |
10.1038/ki.2014.284 |
| リンクURL |
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内容記述タイプ |
Other |
|
内容記述 |
http://www.sciencedirect.com/science/article/pii/S0085253815300570 | http://www.sciencedirect.com/science/article/pii/S0085253815300570 |
| 識別番号 その他 |
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内容記述タイプ |
Other |
|
内容記述 |
PMID:25140913 |
| 抄録 |
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内容記述タイプ |
Abstract |
|
内容記述 |
Bolus administration of endothelin-1 elicits long-lasting renal afferent arteriolar vasoconstriction, in contrast to transient constriction induced by angiotensin II. Vasoconstriction is generally evoked by myosin regulatory light chain (LC20) phosphorylation at Ser19 by myosin light chain kinase (MLCK), which is enhanced by Rho-associated kinase (ROCK)-mediated inhibition of myosin light chain phosphatase (MLCP). LC20 can be diphosphorylated at Ser19 and Thr18, resulting in reduced rates of dephosphorylation and relaxation. Here we tested whether LC20 diphosphorylation contributes to sustained endothelin-1 but not transient angiotensin II-induced vasoconstriction. Endothelin-1 treatment of isolated arterioles elicited a concentration- and time-dependent increase in LC20 diphosphorylation at Thr18 and Ser19. Inhibition of MLCK or ROCK reduced endothelin-1-evoked LC20 mono- and diphosphorylation. Pretreatment with an ETB but not an ETA receptor antagonist abolished LC20 diphosphorylation, and an ETB receptor agonist induced LC20 diphosphorylation. In contrast, angiotensin II caused phosphorylation exclusively at Ser19. Thus, endothelin-1 and angiotensin II induce afferent arteriolar constriction via LC20 phosphorylation at Ser19 due to calcium activation of MLCK and ROCK-mediated inhibition of MLCP. Endothelin-1, but not angiotensin II, induces phosphorylation of LC20 at Thr18. This could contribute to the prolonged vasoconstrictor response to endothelin-1. |
| 注記 |
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内容記述タイプ |
Other |
|
注記 |
CC-BY-NC-ND |
| 資源タイプ |
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|
内容記述タイプ |
Other |
|
資源タイプ |
text |
| 著者版フラグ |
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出版タイプ |
AM |
| フォーマット |
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内容記述タイプ |
Other |
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内容記述 |
application/pdf |
| ID(XooNIps) |
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25140913 |
| 閲覧数(XooNIps) |
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| ダウンロード数(XooNIps) |
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|
1048 |
6385.pdf (2.7 MB)
