『徳島大学 教育・研究者情報データベース (EDB)』---[学外] /
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EID=377919EID:377919, Map:0, LastModified:2021年8月10日(火) 13:02:59, Operator:[大家 隆弘], Avail:TRUE, Censor:承認済, Owner:[田原 強], Read:継承, Write:継承, Delete:継承.
○種別 (必須): □学術論文 (審査論文) [継承]
○言語 (必須): □英語 [継承]
○招待 (推奨):
○審査 (推奨):
○カテゴリ (推奨):
○共著種別 (推奨):
○学究種別 (推奨):
○組織 (推奨):
○著者 (必須): 1. (英) Sasahara Tomoya (日) (読)
○役割 (任意):
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○学籍番号 (推奨):
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2. (英) Yayama Katsutoshi (日) (読)
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3.田原 強 ([徳島大学.先端研究推進センター.バイオイメージング研究部門])
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4. (英) Onoe Hirotaka (日) (読)
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5. (英) Okamoto Hiroshi (日) (読)
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○題名 (必須): □(英) Na+/H+ exchanger inhibitor augments hyperosmolarity-induced vasoconstriction by enhancing actin polymerization.  (日)    [継承]
○副題 (任意):
○要約 (任意): □(英) Vascular smooth muscle cells (VSMCs) exhibit shrinkage-induced activation of Na(+)/H(+) exchanger isoform 1 (NHE-1) and Na(+), K(+), 2Cl(-) cotransporter (NKCC) under hyperosmotic conditions. To investigate the roles of these ion transporters in vascular smooth muscle force induced by hyperosmotic stress, we tested the effects of 5-(N, N-dimethyl)-amiloride (DMA; NHE inhibitor), cariporide (a selective NHE-1 inhibitor), and bumetanide (NKCC inhibitor) on the contractile response of rat aortic rings to hyperosmolar solutions. NHE inhibitors significantly augmented the maximum force response and contractile sensitivity to hyperosmolar sucrose, NaCl, and glucose in endothelium-denuded rings. Bumetanide elicited a comparatively modest increase in sensitivity. NHE inhibitors blocked the increase in intracellular pH and enhanced the cell volume decrease of cultured VSMCs after exposure to hyperosmolar sucrose. However, DMA had no effect on the increase in cytosolic free Ca(2+) concentration ([Ca(2+)]i) in rat VSMCs and on the increases in phosphorylation of myosin phosphatase target subunit 1 and myosin light chain (MLC) in aortic rings in response to hyperosmolar sucrose. Hyperosmolar sucrose-induced force was significantly attenuated by cytochalasin B in the presence or absence of DMA. Exposure to hyperosmolar sucrose increased the ratio of F- to G-actin; the ratio was further elevated by DMA. These results suggest that the potentiation of hyperosmotic shrinkage by NHE inhibition promotes actin polymerization in VSMCs and augments force production independent of changes in [Ca(2+)]i and MLC phosphorylation.  (日)    [継承]
○キーワード (推奨): 1. (英) Actins (日) (読) [継承]
2. (英) Amiloride (日) (読) [継承]
3. (英) Animals (日) (読) [継承]
4. (英) Aorta, Thoracic (日) (読) [継承]
5. (英) Bumetanide (日) (読) [継承]
6. (英) Calcium (日) (読) [継承]
7. (英) Guanidines (日) (読) [継承]
8. (英) Hydrogen-Ion Concentration (日) (読) [継承]
9. (英) Male (日) (読) [継承]
10. (英) Muscle, Smooth, Vascular (日) (読) [継承]
11. (英) Myocytes, Smooth Muscle (日) (読) [継承]
12. (英) Myosin Light Chains (日) (読) [継承]
13. (英) Osmolar Concentration (日) (読) [継承]
14. (英) Phosphorylation (日) (読) [継承]
15. (英) Polymerization (日) (読) [継承]
16. (英) Rats (日) (読) [継承]
17. (英) Rats, Wistar (日) (読) [継承]
18. (英) Sodium-Hydrogen Exchangers (日) (読) [継承]
19. (英) Sodium-Potassium-Chloride Symporters (日) (読) [継承]
20. (英) Sulfones (日) (読) [継承]
21. (英) Vasoconstriction (日) (読) [継承]
○発行所 (推奨):
○誌名 (必須): □Vascular Pharmacology ([Elsevier])
(pISSN: 1537-1891, eISSN: 1879-3649)

○ISSN (任意): □1879-3649
ISSN: 1537-1891 (pISSN: 1537-1891, eISSN: 1879-3649)
Title: Vascular pharmacology
Title(ISO): Vascul Pharmacol
Publisher: Elsevier Inc.
 (NLM Catalog)   (Scopus)   (CrossRef)  (Scopus information is found. [need login])
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○巻 (必須): □59 [継承]
○号 (必須): □5-6 [継承]
○頁 (必須): □120 126 [継承]
○都市 (任意):
○年月日 (必須): □西暦 2013年 7月 19日 (平成 25年 7月 19日) [継承]
○URL (任意):
○DOI (任意): □10.1016/j.vph.2013.07.004    (→Scopusで検索) [継承]
○PMID (任意): □23872622    (→Scopusで検索) [継承]
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○備考 (任意): 1.(英) PublicationType: Journal Article  (日)    [継承]

標準的な表示

和文冊子 ● Tomoya Sasahara, Katsutoshi Yayama, Tsuyoshi Tahara, Hirotaka Onoe and Hiroshi Okamoto : Na+/H+ exchanger inhibitor augments hyperosmolarity-induced vasoconstriction by enhancing actin polymerization., Vascular Pharmacology, Vol.59, No.5-6, 120-126, 2013.
欧文冊子 ● Tomoya Sasahara, Katsutoshi Yayama, Tsuyoshi Tahara, Hirotaka Onoe and Hiroshi Okamoto : Na+/H+ exchanger inhibitor augments hyperosmolarity-induced vasoconstriction by enhancing actin polymerization., Vascular Pharmacology, Vol.59, No.5-6, 120-126, 2013.

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