Sodium-coupled glucose transporter as a functional glucose sensor of retinal microvascular circulation

Masanori Wakisaka, Takanari Kitazono, Masako Kato, Udai Nakamura, Maki Yoshioka, Yuji Uchizono, Mototaka Yoshinari

研究成果: Contribution to journalArticle査読

18 被引用数 (Scopus)

抄録

To clarify the function of the Na+-coupled glucose transporter in the regulation of cellular tone of cultured retinal pericytes, we investigated the effects of extracellular glucose concentration on cell size. The surface area and diameter of cultured bovine retinal pericytes under different glucose concentrations were measured by using a light microscope with a digital camera. We also examined the effects of extracellular Na+ and Ca2+, inhibitors of the Na+-coupled glucose transporter and Na+-Ca2+ exchanger, a Ca2+ channel blocker, and nonmetabolizable sugars on cell size. The surface area and diameter of the cells changed according to extracellular glucose concentrations. α-Methyl glucoside, which enters the cell through the Na+-coupled glucose transporter, induced cellular contraction. However, the cells did not contract in response to 2-deoxyglucose, which enters the cell through a facilitated glucose transporter. Glucose-induced cellular contraction was abolished in the absence of extracellular Na+ and Ca2+. Moreover, phlorizin, an inhibitor of the Na+-coupled glucose transporter, and 2′,4′-dichlorobenzamil-HCl, an inhibitor of the Na+-Ca2+ exchanger, also abolished glucose-induced cellular contraction, whereas nicardipine, a Ca2+ channel blocker, did not. Our results indicate that high extracellular glucose concentrations induce contraction of bovine retinal pericytes via Na+ entry through a Na+-coupled glucose transporter, suggesting that the Na+-coupled glucose transporter may act as a functional glucose sensor of retinal microvascular circulation.

本文言語英語
ページ(範囲)1183-1188
ページ数6
ジャーナルCirculation research
88
11
DOI
出版ステータス出版済み - 6 8 2001

All Science Journal Classification (ASJC) codes

  • 生理学
  • 循環器および心血管医学

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