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Am J Physiol Cell Physiol 277: C343-C349, 1999;
0363-6143/99 $5.00
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Vol. 277, Issue 2, C343-C349, August 1999

Cell proliferation is associated with enhanced capacitative Ca2+ entry in human arterial myocytes

Vera A. Golovina

Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Depletion of Ca2+ stores in the sarcoplasmic reticulum (SR) activates extracellular Ca2+ influx via capacitative Ca2+ entry (CCE). Here, CCE levels in proliferating and growth-arrested human pulmonary artery smooth muscle cells (PASMCs) were compared by digital imaging fluorescence microscopy. Resting cytosolic free Ca2+ concentration ([Ca2+]cyt) in proliferating PASMCs was twofold higher than that in growth-arrested cells. Cyclopiazonic acid (CPA; 10 µM), which inhibits SR Ca2+-ATPase and depletes inositol 1,4,5-trisphosphate-sensitive Ca2+ stores, transiently increased [Ca2+]cyt in the absence of extracellular Ca2+. The addition of 1.8 mM Ca2+ to the extracellular solution in the presence of CPA induced large increases in [Ca2+]cyt, indicative of CCE. The CPA-induced SR Ca2+ release in proliferating PASMCs was twofold higher than that in growth-arrested cells, whereas the transient rise of [Ca2+]cyt due to CCE was fivefold greater in proliferating cells. CCE was insensitive to nifedipine but was significantly inhibited by 50 mM K+, which reduces the driving force for Ca2+ influx, and by 0.5 mM Ni2+, a putative blocker of store-operated Ca2+ channels. These data show that augmented CCE is associated with proliferation of human PASMCs and may be involved in stimulating and maintaining cell growth.

vascular smooth muscle cells; growth factors; sarcoplasmic reticulum; digital imaging; fura 2


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