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Articles in PresS, published online ahead of print October 9, 2002
Am J Physiol Cell Physiol, 10.1152/ajpcell.00260.2002
Submitted on June 4, 2002
Accepted on September 30, 2002
1 Cardiovascular Sciences, Albany Medical College, Albany, NY, USA
2 Biomedical Sciences, Cornell University, Ithaca, NY, USA
* To whom correspondence should be addressed. E-mail: wangy{at}mail.amc.edu.
We examined the effects of metabolic inhibition on intracellular Ca2+ release in single pulmonary arterial smooth muscle cells (PASMCs). Severe metabolic inhibition with cyanide (CN, 10 mM) increased [Ca2+]i and activated Ca2+-activated Cl- currents (ICl(Ca)) in PASMCs, responses that were greatly inhibited by BAPTA/AM or caffeine. Mild metabolic inhibition with CN (1 mM) increased spontaneous transient inward currents and Ca2+ sparks in PASMCs. In Xenopus oocytes CN also induced Ca2+ release and activated ICl(Ca), and these responses were inhibited by thapsigargin and cyclopiazonic acid to deplete SR Ca2+, whereas neither heparin nor anti-IP3R antibodies affected CN responses. In both PASMCs and oocytes, cyanide -evoked Ca2+ release was inhibited by carbonyl cyanide m-chlorophenylhydrazone (CCCP) and oligomycin or CCCP and thapsigargin. 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 with CN increases [Ca2+]i in both pulmonary and systemic artery myocytes by stimulating Ca2+ release from the SR and mitochondria.
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