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Am J Physiol Heart Circ Physiol 280: H1002-H1010, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 3, H1002-H1010, March 2001

Modulation of early [Ca2+]i rise in metabolically inhibited endothelial cells by xestospongin C

M. Schäfer, D. Bahde, B. Bosche, Y. Ladilov, C. Schäfer, H. M. Piper, and T. Noll

Physiologisches Institut, Justus-Liebig-Universität, D-35392 Giessen, Germany

When energy metabolism is disrupted, endothelial cells lose Ca2+ from endoplasmic reticulum (ER) and the cytosolic Ca2+ concentration ([Ca2+]i) increases. The importance of glycolytic energy production and the mechanism of Ca2+ loss from the ER were analyzed. Endothelial cells from porcine aorta in culture and in situ were used as models. 2-Deoxy-D-glucose (2-DG, 10 mM), an inhibitor of glycolysis, caused an increase in [Ca2+]i (measured with fura 2) within 1 min when total cellular ATP contents were not yet affected. Stimulation of oxidative energy production with pyruvate (5 mM) did not attenuate this 2-DG-induced rise of [Ca2+]i, while this maneuver preserved cellular ATP contents. The inhibitor of ER-Ca2+-ATPase, thapsigargin (10 nM), augmented the 2-DG-induced rise of [Ca2+]i. Xestospongin C (3 µM), an inhibitor of D-myo-inositol 3-phosphate [Ins(3)P]-sensitive ER-Ca2+ release, abolished the rise. The results demonstrate that the ER of endothelial cells is very sensitive to glycolytic metabolic inhibition. When this occurs, the ER Ca2+ store is discharged by opening of the Ins(3)P-sensitive release channel. Xestospongin C can effectively suppress the early [Ca2+]i rise in metabolically inhibited endothelial cells.

D-myo-inositol 3-phosphate-sensitive Ca2+ release; ischemia; hypoxia; cytosolic Ca2+ concentration


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