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Am J Physiol Heart Circ Physiol 283: H382-H390, 2002. First published March 28, 2002; doi:10.1152/ajpheart.00574.2001
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Vol. 283, Issue 1, H382-H390, July 2002

Superoxide anion impairs contractility in cultured aortic smooth muscle cells

Chiwaka Kimura, Wei Cheng, Kazunari Hisadome, Yi-Ping Wang, Tetsuya Koyama, Yuji Karashima, Masahiro Oike, and Yushi Ito

Department of Pharmacology, Graduate School of Medical Sciences, Kyushu University, Fukuoka 812-8582, Japan

We examined the effects of superoxide anion (O<UP><SUB>2</SUB><SUP>−</SUP></UP>) generated by xanthine plus xanthine oxidase (X/XO) on the intracellular Ca2+ concentration ([Ca2+]i) and muscle contractility in cultured bovine aortic smooth muscle cells (BASMC). Cells were grown on collagen-coated dish for the measurement of [Ca2+]i. Pretreatment with X/XO inhibited ATP-induced Ca2+ transient and Ca2+ release-activated Ca2+ entry (CRAC) after thapsigargin-induced store depletion, both of which were reversed by superoxide dismutase (SOD). In contrast, Ca2+ transients induced by high-K+ solution and Ca2+ ionophore A-23187 were not affected by X/XO. BASMC-embedded collagen gel lattice, which was pretreated with xanthine alone, showed contraction in response to ATP, thapsigargin, high-K+ solution, and A-23187. Pretreatment of the gel with X/XO impaired gel contraction not only by ATP and thapsigargin, but also by high-K+ solution and A-23187. The X/XO-treated gel showed normal contraction; however, when SOD was present during the pretreatment period. These results indicate that O<UP><SUB>2</SUB><SUP>−</SUP></UP> attenuates smooth muscle contraction by impairing CRAC, ATP-induced Ca2+ transient, and Ca2+ sensitivity in BASMC.

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