Circulation Research. 1996;79:909-910
(Circulation Research. 1996;79:909-910.)
© 1996 American Heart Association, Inc.
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
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Introduction
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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 [Ca
2+]
i (Ca
2+ transients) are important
for the regulation of intracellular processes, and when these
Ca
2+ transients are propagated as Ca
2+ waves, they may influence
or regulate signaling between cells and through tissues. Intracellular
and intercellular Ca
2+ 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 Ca
2+ waves have been observed
predominantly in excitable cells
1 (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
Ca
2+ waves, although they do show occasional sporadic Ca
2+ oscillations.
4 5 6 Therefore, the prevailing view of Ca
2+ regulation in pulmonary
endothelial cells is that [Ca
2+]
i is relatively uniform in the
absence of chemical agonists or mechanical stimulation. However,
the article by Ying et al
7 in this issue of
Circulation Research challenges these rather simple notions of Ca
2+ homeostasis in
pulmonary endothelium and suggests a degree of complexity in
Ca
2+ 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]