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Characterization of hypoxia-induced [Ca2+](i) rise in rabbit pulmonary arterial smooth muscle cells

机译:缺氧诱导兔肺动脉平滑肌细胞[Ca2 +](i)升高的特征

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;e have investigated the effects of hypoxia on the intracellular Ca2+ concentration ([Ca2+](i)) in rabbit pulmonary (PASMCs) and coronary arterial smooth muscle cells with fura-2. Perfusion of a glucose-free and hypoxic (P-O2<50 mmHg) external solution increased [Ca2+](i) in cultured as well as freshly isolated PASMCs. However it had no effect on [Ca2+](i) in freshly isolated coronary arterial myocytes. In the absence of extracellular Ca2+, hypoxic stimulation elicited a transient [Ca2+](i) increase in cultured PASMCs which was abolished by the simultaneous application of cyclopiazonic acid and ryanodine, suggesting the involvement of sarcoplasmic reticulum (SR) Ca2+ store. Pretreatment with the mitochondrial protonophore, carbonyl cyanide m-chlorophenyl-hydrazone (CCCP) enhanced the [Ca2+](i) rise in response to hypoxia. A short application of caffeine gave a transient [Ca2+](i) rise which was prolonged by CCCP. Decay of the caffeine-induced [Ca2+](i) transients was significantly slowed by treatment of CCCP or rotenone. After full development of the hypoxia-induced [Ca2+](i) rise, nifedipine did not decrease [Ca2+](i). These data suggest that the [Ca2+](i) increase in response to hypoxia may be ascribed to both Ca2+ release from the SR and the subsequent activation of nifedipine-insensitive capacitative Ca2+ entry. Mitochondria appear to modulate hypoxia induced Ca2+ release from the SR. (C) 2002 Elsevier Science Inc. All rights reserved. [References: 30]
机译:; e研究了低氧对呋喃2引起的兔肺(PASMC)和冠状动脉平滑肌细胞内Ca2 +浓度([Ca2 +](i))的影响。在培养以及新鲜分离的PASMC中,无葡萄糖和低氧(P-O2 <50 mmHg)外部溶液的灌注增加[Ca2 +](i)。但是,它对新鲜分离的冠状动脉心肌细胞中的[Ca2 +](i)没有影响。在不存在细胞外Ca2 +的情况下,低氧刺激在培养的PASMC中引起瞬时[Ca2 +](i)升高,但同时应用环吡嗪酸和ryanodine可以消除这种升高,这表明肌浆网(SR)Ca2 +的参与。用线粒体质子载体预处理,羰基氰化物间氯苯基phenyl(CCCP)增强了缺氧引起的[Ca2 +](i)升高。短时间使用咖啡因会导致短暂的[Ca2 +](i)升高,而CCCP则将其延长。通过CCCP或鱼藤酮的处理,咖啡因诱导的[Ca2 +](i)瞬变的衰减显着减慢。缺氧诱导的[Ca2 +](i)升高完全发展后,硝苯地平未降低[Ca2 +](i)。这些数据表明,对缺氧反应的[Ca2 +](i)升高可能归因于SR中Ca2 +的释放以及硝苯地平不敏感的电容性Ca2 +进入的随后激活。线粒体似乎可以调节缺氧诱导的SR释放Ca2 +。 (C)2002 Elsevier Science Inc.保留所有权利。 [参考:30]

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