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Am J Physiol Heart Circ Physiol 275: H844-H851, 1998;
0363-6135/98 $5.00
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Vol. 275, Issue 3, H844-H851, September 1998

Ablation of lung endothelial injury after pacing-induced heart failure is related to alterations in Ca2+ signaling

Claire L. Ivey, Beverly J. Roy, and Mary I. Townsley

Department of Physiology, University of South Alabama, Mobile, Alabama 36688

We have previously shown that ANG II increases microvascular permeability in normal dog lungs but not after pacing-induced heart failure. This study investigated how ANG II induces permeability in isolated blood-perfused canine lung lobes and what alterations occur during heart failure. In normal lobes, the protein kinase C (PKC) inhibitors staurosporine (500 nM) or chelerythrine (10 µM) did not modify ANG II-induced increases in the capillary filtration coefficient (Kf,c, ml · min-1 · cmH2O-1 · 100 g-1; an index of microvascular permeability), suggesting that PKC is not involved. Thapsigargin (150 nM) was used to stimulate capacitative Ca2+ entry in lobes from control dogs and dogs paced at 245 beats/min for 4 wk to induce heart failure. In control lobes, Kf,c rose after thapsigargin, from 0.06 ± 0.01 to 0.17 ± 0.03 ml · min-1 · cmH2O-1 · 100 g-1 (mean ± SE, P < 0.05) but did not change in the paced group. A Ca2+ ionophore, A-23187, increased Kf,c in both control (10 µM; 0.05 ± 0.01 to 0.17 ± 0.05 ml · min-1 · cmH2O-1 · 100 g-1, P < 0.05) and pace (5 µM; 0.06 ± 0.01 to 0.21 ± 0.07 ml · min-1 · cmH2O-1 · 100 g-1, P < 0.05) lobes, indicating that increasing intracellular Ca2+ is sufficient to induce pulmonary microvascular permeability after pacing. We conclude that during heart failure, Ca2+ signaling within the pulmonary microvascular endothelium is altered.

venous hypertension; microvascular permeability; capacitative calcium entry; pulmonary endothelium; capillary filtration coefficient


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