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Articles in PresS, published online ahead of print March 28, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00574.2001
Submitted on July 2, 2001
Accepted on March 21, 2002
1 Pharmacology, Kyushu University, Graduate School of Medical Sciences, Fukuoka, Fukuoka, Japan
2 Pharmacology, Jinzhou Medical College, Jinzhou, China
3 Pharmacology, Shanghai Institute of Materia Medica, Shanghai, China
* To whom correspondence should be addressed. E-mail: moike{at}pharmaco.med.kyushu-u.ac.jp.
We examined the effects of superoxide anion (O2-), generated by xanthine (X) and xanthine oxidase (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 A23187 were not affected by X/XO. BASMC-embedded collagen gel lattice, which was pretreated with X alone, showed contraction in response to ATP, thapsigargin, high K+ solution and A23187. Pretreatment of the gel with X/XO impaired gel contraction not only by ATP and thapsigargin but also by high K+ and A23187. The X/XO-treated gel showed normal contraction, however, when SOD was present during the pretreatment period. These results indicate that O2- attenuates smooth muscle contraction by impairing CRAC, ATP-induced Ca2+ transient and Ca2+ sensitivity in BASMC.
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