Inhibition of glycolysis by 2-DG increases [Ca2+](i) in pulmonary arterial smooth muscle cells

R. T. Bright, C. G. Salvaterra, L. J. Rubin, X. J. Yuan

Research output: Contribution to journalArticlepeer-review

25 Scopus citations


Inhibition of glycolysis depolarizes single pulmonary arterial smooth muscle cells (PASMC) and potentiates hypoxic pulmonary vasoconstriction (HPV) in isolated perfused rat lungs. Whether glycolytic inhibition causes an increase in the intracellular Ca2+ concentration ([Ca2+](i)) in PASMC was determined in this study. [Ca2+](i) was measured in primary cultured rat PASMC using the Ca2+-sensitive fluorescent indicator, fura 2, and quantitative fluorescence microscopy. Extracellular application of the glycolytic inhibitor, 2-deoxy-D-glucose (2-DG), significantly and reversibly increased [Ca2+](i) in PASMC. Removal of extracellular Ca2+ and application of the Ca2+ channel blocker, verapamil (10 μM), attenuated, but did not eliminate, the 2-DG-induced rise in [Ca2+](i). In the absence of extracellular Ca2+, however, depletion of inositol triphosphate- sensitive intracellular Ca2+ stores by 10 μM cyclopiazonic acid (CPA) completely abolished the 2-DG-induced increase in [Ca2+](i). The data suggest that 2-DG-induced increases in [Ca2+](i) result from both Ca2+ influx through the verapamil-sensitive voltage-gated Ca2+ channels and Ca2+ release from the CPA-sensitive intracellular Ca2+ stores.

Original languageEnglish (US)
Pages (from-to)L203-L208
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number2 13-2
StatePublished - 1995
Externally publishedYes


  • 2-deoxy-D-glucose
  • intracellular calcium

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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