AJP - Heart Calcium Transients and Cell-Sarcomere
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Am J Physiol Heart Circ Physiol 279: H1625-H1634, 2000;
0363-6135/00 $5.00
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Vol. 279, Issue 4, H1625-H1634, October 2000

VEGF and ATP act by different mechanisms to increase microvascular permeability and endothelial [Ca2+]i

T. M. Pocock1, B. Williams2, F. E. Curry3, and D. O. Bates1,2

1 Department of Physiology, University of Bristol, Bristol BS2 8EJ; 2 Cardiovascular Research Institute, University of Leicester, Leicester, LE2 7LX United Kingdom; and 3 Department of Human Physiology, University of California at Davis, Davis, California 95616

Vascular endothelial growth factor (VEGF) increases hydraulic conductivity (Lp) by stimulating Ca2+ influx into endothelial cells. To determine whether VEGF-mediated Ca2+ influx is stimulated by release of Ca2+ from intracellular stores, we measured the effect of Ca2+ store depletion on VEGF-mediated increased Lp and endothelial intracellular Ca2+ concentration ([Ca2+]i) of frog mesenteric microvessels. Inhibition of Ca2+ influx by perfusion with NiCl2 significantly attenuated VEGF-mediated increased [Ca2+]i. Depletion of Ca2+ stores by perfusion of vessels with thapsigargin did not affect the VEGF-mediated increased [Ca2+]i or the increase in Lp. In contrast, ATP-mediated increases in both [Ca2+]i and Lp were inhibited by thapsigargin perfusion, demonstrating that ATP stimulated store-mediated Ca2+ influx. VEGF also increased Mn2+ influx after perfusion with thapsigargin, whereas ATP did not. These data showed that VEGF increased [Ca2+]i and Lp even when Ca2+ stores were depleted and under conditions that prevented ATP-mediated increases in [Ca2+]i and Lp. This suggests that VEGF acts through a Ca2+ store-independent mechanism, whereas ATP acts through Ca2+ store-mediated Ca2+ influx.

vascular endothelial growth factor; vascular permeability; endothelial calcium; calcium stores; intracellular calcium concentration; adenosine 5'-triphosphate


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