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Circulation Research. 1996;79:909-910

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(Circulation Research. 1996;79:909-910.)
© 1996 American Heart Association, Inc.


Articles

Spontaneous Ca2+ Oscillations and Waves in Pulmonary Vascular Endothelial Cells

C. William Balke

the Department of Physiology and Department of Medicine, Division of Cardiology, University of Maryland School of Medicine, Baltimore, Md.

Correspondence to C. William Balke, MD, University of Maryland School of Medicine, Department of Physiology, Howard Hall, Room 560, 660 W Redwood St, Baltimore, MD 21201. E-mail bbalke@heart/ab/umd/edu.


Key Words: Ca2+ • Ca2+ oscillations • Ca2+ wave • pulmonary endothelial cell • fura 2


*    Introduction
 
Calcium is a ubiquitous second messenger that regulates a number of cellular processes in both excitable and nonexcitable cells.1 2 3 Transient elevations in [Ca2+]i (Ca2+ transients) are important for the regulation of intracellular processes, and when these Ca2+ transients are propagated as Ca2+ waves, they may influence or regulate signaling between cells and through tissues. Intracellular and intercellular Ca2+ waves have been observed in a variety of cell types and are initiated principally by two types of mechanisms: (1) stimulus-mediated mechanisms (eg, chemical agonist, electrical, or mechanical stimuli) and (2) spontaneously occurring mechanisms. In general, spontaneous Ca2+ waves have been observed predominantly in excitable cells1 (eg, skeletal, cardiac, and vascular smooth muscle cells). Nonexcitable cells, such as endothelial cells, which have been studied principally in isolation or in cell culture preparations, do not show typically spontaneous Ca2+ waves, although they do show occasional sporadic Ca2+ oscillations.4 5 6 Therefore, the prevailing view of Ca2+ regulation in pulmonary endothelial cells is that [Ca2+]i is relatively uniform in the absence of chemical agonists or mechanical stimulation. However, the article by Ying et al7 in this issue of Circulation Research challenges these rather simple notions of Ca2+ homeostasis in pulmonary endothelium and suggests a degree of complexity in Ca2+ signaling similar to that found in excitable cells.

The novel findings of these investigators are due, in large part, to their ability to measure intracellular Ca2+ transients in individual endothelial cells in an in situ model of endothelial cell function (ie, venular capillaries of the . . . [Full Text of this Article]