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Departments of Medicine, and of Physiology and Cellular Biophysics, College of Physicians and Surgeons, Columbia University; and St. Luke's-Roosevelt Hospital Center, New York, New York 10019
Endothelial second messenger responses may contribute to the pathology of high vascular pressure but remain poorly understood because of the lack of direct in situ quantification. In lung venular capillaries, we determined endothelial cytosolic Ca2+ concentration [Ca2+]i by the fura 2 ratioing method. Pressure elevation increased mean endothelial [Ca2+]i by Ca2+ influx through gadolinium-inhibitable channels and amplified [Ca2+]i oscillations by Ca2+ release from intracellular stores. Endothelial [Ca2+]i transients were induced by pressure elevations of as little as 5 cmH2O and increased linearly with higher pressures. Heptanol inhibition of [Ca2+]i oscillations in a subset of endothelial cells indicated that oscillations originated from pacemaker endothelial cells and were propagated to adjacent nonpacemaker cells by gap junctional communication. Our findings indicate the presence of a sensitive, active endothelial response to pressure challenge in lung venular capillaries that may be relevant in the pathogenesis of pressure-induced lung microvascular injury.
pulmonary; endothelium; calcium; hydrostatic pressure
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