Inhibition of glycolysis by 2-dog increases [ca2+]i in pulmonary
arterial smooth muscle cells.
Bright, Rose T., Carmen G. Salvaterra, Lewis J. Rubin, and Xiao-Jian
Yuan.
Department of Medicine, Division of Pulmonary and Critical Care
Medicine, Department of Physiology, University of Maryland School of
Medicine, Baltimore, Maryland 21201
APStracts 2:0056L, 1995.
Inhibition of glycolysis depolarizes single 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 pulmonary arterial
smooth muscle cells (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-DOG), significantly and reversibly increased
[Ca2+]i in PASMC. Removal of extracellular Ca2+ and application of
the Ca2+ channel blocker, verapamil (10 [mu]M), attenuated, but did
not eliminate, the 2-DOG-induced rise in [Ca2+]i. In the absence of
extracellular Ca2+, however, depletion of inositol triphosphate
-sensitive intracellular Ca2+ stores by 10 [mu]M cyclopiazonic acid
(CPA) completely abolished the 2-DOG-induced increase in [Ca2+]i. The
data suggest that 2-DOG-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.
Received 1 December 1994; accepted in final form 6 April 1995.
APS Manuscript Number L341-4.
Article publication pending Am. J. Physiol. (Lung Cell. Mol.
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 25 April 1995.