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Am J Physiol Lung Cell Mol Physiol 278: L261-L267, 2000;
1040-0605/00 $5.00
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Vol. 278, Issue 2, L261-L267, February 2000

High K+-induced membrane depolarization attenuates endothelium-dependent pulmonary vasodilation

Jan E. Seiden1, Oleksandr Platoshyn2, Alan E. Bakst1, Sharon S. McDaniel2, and Jason Xiao-Jian Yuan2

1 Department of Medicine, University of Maryland School of Medicine, Baltimore, Maryland 21201; and 2 Department of Medicine, University of California, San Diego, California 92103-8382

Impairment of endothelium-dependent pulmonary vasodilation has been implicated in the development of pulmonary hypertension. Pulmonary vascular smooth muscle cells and endothelial cells communicate electrically through gap junctions; thus, membrane depolarization in smooth muscle cells would depolarize endothelial cells. In this study, we examined the effect of prolonged membrane depolarization induced by high K+ on the endothelium-dependent pulmonary vasodilation. Isometric tension was measured in isolated pulmonary arteries (PA) from Sprague-Dawley rats, and membrane potential was measured in single PA smooth muscle cells. Increase in extracellular K+ concentration from 4.7 to 25 mM significantly depolarized PA smooth muscle cells. The 25 mM K+-mediated depolarization was characterized by an initial transient depolarization (5-15 s) followed by a sustained depolarization that could last for up to 3 h. In endothelium-intact PA rings, ACh (2 µM), levcromakalim (10 µM), and nitroprusside (10 µM) reversibly inhibited the 25 mM K+-mediated contraction. Functional removal of endothelium abolished the ACh-mediated relaxation but had no effect on the levcromakalim- or the nitroprusside-mediated pulmonary vasodilation. Prolonged (~3 h) membrane depolarization by 25 mM K+ significantly inhibited the ACh-mediated PA relaxation (-55 ± 4 vs. -29 ± 2%, P < 0.001), negligibly affected the levcromakalim-mediated pulmonary vasodilation (-92 ± 4 vs. -95 ± 5%), and slightly but significantly increased the nitroprusside-mediated PA relaxation (-80 ± 2 vs. 90 ± 3%, P < 0.05). These data indicate that membrane depolarization by prolonged exposure to high K+ concentration selectively inhibited endothelium-dependent pulmonary vasodilation, suggesting that membrane depolarization plays a role in the impairment of pulmonary endothelial function in pulmonary hypertension.

membrane potential; pulmonary circulation


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