Intracellular alkalinization induces Ca2+ influx via non-voltage-operated Ca2+ channels in rat aortic smooth muscle cells

Wakako Eto, Katsuya Hirano, Mayumi Hirano, Junji Nishimura, Hideo Kanaide

研究成果: ジャーナルへの寄稿記事

17 引用 (Scopus)

抄録

In smooth muscle, the cytosolic Ca2+ concentration ([Ca2+]i) is the primary determinant of contraction, and the intracellular pH (pHi) modulates contractility. Using fura-2 and 2′,7′-biscarboxyethyl-5(6) carboxyfluorescein (BCECF) fluorometry and rat aortic smooth muscle cells in primary culture, we investigated the effect of the increase in pHi on [Ca2+]i. The application of the NH4Cl induced concentration-dependent increases in both pHi and [Ca2+]i. The extent of [Ca2+]i elevation induced by 20 mM NH4Cl was approximately 50% of that obtained with 100 mM K+-depolarization. The NH4Cl-induced elevation of [Ca2+]i was completely abolished by the removal of extracellular Ca2+ or the addition of extracellular Ni2+. The 100 mM K+-induced [Ca2+]i elevation was markedly inhibited by a voltage-operated Ca2+ channel blocker, diltiazem, and partly inhibited by a non-voltage-operated Ca2+ channel blocker, SKF96365. On the other hand, the NH4Cl-induced [Ca2+]i elevation was resistant to diltiazem, but was markedly inhibited by SKF96365. It is thus concluded that intracellular alkalinization activates the Ca2+ influx via non-voltage-operated Ca2+ channels and thereby increases [Ca2+]i in the vascular smooth muscle cells. The alkalinization-induced Ca2+ influx may therefore contribute to the enhancement of contraction.

元の言語英語
ページ(範囲)477-484
ページ数8
ジャーナルCell Calcium
34
発行部数6
DOI
出版物ステータス出版済み - 1 1 2003

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1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
Diltiazem
Smooth Muscle Myocytes
Fluorometry
Fura-2
Vascular Smooth Muscle
Smooth Muscle

All Science Journal Classification (ASJC) codes

  • Physiology
  • Molecular Biology
  • Cell Biology

これを引用

Intracellular alkalinization induces Ca2+ influx via non-voltage-operated Ca2+ channels in rat aortic smooth muscle cells. / Eto, Wakako; Hirano, Katsuya; Hirano, Mayumi; Nishimura, Junji; Kanaide, Hideo.

:: Cell Calcium, 巻 34, 番号 6, 01.01.2003, p. 477-484.

研究成果: ジャーナルへの寄稿記事

Eto, Wakako ; Hirano, Katsuya ; Hirano, Mayumi ; Nishimura, Junji ; Kanaide, Hideo. / Intracellular alkalinization induces Ca2+ influx via non-voltage-operated Ca2+ channels in rat aortic smooth muscle cells. :: Cell Calcium. 2003 ; 巻 34, 番号 6. pp. 477-484.
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title = "Intracellular alkalinization induces Ca2+ influx via non-voltage-operated Ca2+ channels in rat aortic smooth muscle cells",
abstract = "In smooth muscle, the cytosolic Ca2+ concentration ([Ca2+]i) is the primary determinant of contraction, and the intracellular pH (pHi) modulates contractility. Using fura-2 and 2′,7′-biscarboxyethyl-5(6) carboxyfluorescein (BCECF) fluorometry and rat aortic smooth muscle cells in primary culture, we investigated the effect of the increase in pHi on [Ca2+]i. The application of the NH4Cl induced concentration-dependent increases in both pHi and [Ca2+]i. The extent of [Ca2+]i elevation induced by 20 mM NH4Cl was approximately 50{\%} of that obtained with 100 mM K+-depolarization. The NH4Cl-induced elevation of [Ca2+]i was completely abolished by the removal of extracellular Ca2+ or the addition of extracellular Ni2+. The 100 mM K+-induced [Ca2+]i elevation was markedly inhibited by a voltage-operated Ca2+ channel blocker, diltiazem, and partly inhibited by a non-voltage-operated Ca2+ channel blocker, SKF96365. On the other hand, the NH4Cl-induced [Ca2+]i elevation was resistant to diltiazem, but was markedly inhibited by SKF96365. It is thus concluded that intracellular alkalinization activates the Ca2+ influx via non-voltage-operated Ca2+ channels and thereby increases [Ca2+]i in the vascular smooth muscle cells. The alkalinization-induced Ca2+ influx may therefore contribute to the enhancement of contraction.",
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T1 - Intracellular alkalinization induces Ca2+ influx via non-voltage-operated Ca2+ channels in rat aortic smooth muscle cells

AU - Eto, Wakako

AU - Hirano, Katsuya

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AU - Nishimura, Junji

AU - Kanaide, Hideo

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N2 - In smooth muscle, the cytosolic Ca2+ concentration ([Ca2+]i) is the primary determinant of contraction, and the intracellular pH (pHi) modulates contractility. Using fura-2 and 2′,7′-biscarboxyethyl-5(6) carboxyfluorescein (BCECF) fluorometry and rat aortic smooth muscle cells in primary culture, we investigated the effect of the increase in pHi on [Ca2+]i. The application of the NH4Cl induced concentration-dependent increases in both pHi and [Ca2+]i. The extent of [Ca2+]i elevation induced by 20 mM NH4Cl was approximately 50% of that obtained with 100 mM K+-depolarization. The NH4Cl-induced elevation of [Ca2+]i was completely abolished by the removal of extracellular Ca2+ or the addition of extracellular Ni2+. The 100 mM K+-induced [Ca2+]i elevation was markedly inhibited by a voltage-operated Ca2+ channel blocker, diltiazem, and partly inhibited by a non-voltage-operated Ca2+ channel blocker, SKF96365. On the other hand, the NH4Cl-induced [Ca2+]i elevation was resistant to diltiazem, but was markedly inhibited by SKF96365. It is thus concluded that intracellular alkalinization activates the Ca2+ influx via non-voltage-operated Ca2+ channels and thereby increases [Ca2+]i in the vascular smooth muscle cells. The alkalinization-induced Ca2+ influx may therefore contribute to the enhancement of contraction.

AB - In smooth muscle, the cytosolic Ca2+ concentration ([Ca2+]i) is the primary determinant of contraction, and the intracellular pH (pHi) modulates contractility. Using fura-2 and 2′,7′-biscarboxyethyl-5(6) carboxyfluorescein (BCECF) fluorometry and rat aortic smooth muscle cells in primary culture, we investigated the effect of the increase in pHi on [Ca2+]i. The application of the NH4Cl induced concentration-dependent increases in both pHi and [Ca2+]i. The extent of [Ca2+]i elevation induced by 20 mM NH4Cl was approximately 50% of that obtained with 100 mM K+-depolarization. The NH4Cl-induced elevation of [Ca2+]i was completely abolished by the removal of extracellular Ca2+ or the addition of extracellular Ni2+. The 100 mM K+-induced [Ca2+]i elevation was markedly inhibited by a voltage-operated Ca2+ channel blocker, diltiazem, and partly inhibited by a non-voltage-operated Ca2+ channel blocker, SKF96365. On the other hand, the NH4Cl-induced [Ca2+]i elevation was resistant to diltiazem, but was markedly inhibited by SKF96365. It is thus concluded that intracellular alkalinization activates the Ca2+ influx via non-voltage-operated Ca2+ channels and thereby increases [Ca2+]i in the vascular smooth muscle cells. The alkalinization-induced Ca2+ influx may therefore contribute to the enhancement of contraction.

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