Metabolic inhibition with cyanide induces calcium release in pulmonary artery myocytes and Xenopus oocytes |
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Authors: | Wang Yong-Xiao Zheng Yun-Min Abdullaev Iskandar Kotlikoff Michael I |
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Institution: | Center for Cardiovascular Sciences, Albany Medical College, Albany 12208, USA. wangy@mail.amc.edu |
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Abstract: | We examined the effectsof metabolic inhibition on intracellular Ca2+ release insingle pulmonary arterial smooth muscle cells (PASMCs). Severemetabolic inhibition with cyanide (CN, 10 mM) increased intracellularcalcium concentration (Ca2+]i) and activatedCa2+-activated Cl currentsICl(Ca)] in PASMCs, responses that were greatlyinhibited by BAPTA-AM or caffeine. Mild metabolic inhibition with CN (1 mM) increased spontaneous transient inward currents andCa2+ sparks in PASMCs. In Xenopus oocytes, CNalso induced Ca2+ release and activatedICl(Ca), and these responses were inhibited by thapsigarginand cyclopiazonic acid to deplete sarcoplasmic reticulum (SR)Ca2+, whereas neither heparin nor anti-inositol1,4,5-trisphosphate receptor (IP3R) antibodies affected CNresponses. In both PASMCs and oocytes, CN-evoked Ca2+release was inhibited by carbonyl cyanidem-chlorophenylhydrazone (CCCP) and oligomycin or CCCP andthapsigargin. Whereas hypoxic stimuli resulted in Ca2+release in pulmonary but not mesenteric artery myocytes, CN induced release in both cell types. We conclude that metabolic inhibition withCN increases Ca2+]i in both pulmonary andsystemic artery myocytes by stimulating Ca2+ release fromthe SR and mitochondria. |
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