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Am J Physiol Lung Cell Mol Physiol 279: L884-L894, 2000;
1040-0605/00 $5.00
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Vol. 279, Issue 5, L884-L894, November 2000

L-type Ca2+ channels, resting [Ca2+]i, and ET-1-induced responses in chronically hypoxic pulmonary myocytes

Larissa A. Shimoda, James S. K. Sham, Tenille H. Shimoda, and J. T. Sylvester

Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins University, Baltimore, Maryland 21224

In the lung, chronic hypoxia (CH) causes pulmonary arterial smooth muscle cell (PASMC) depolarization, elevated endothelin-1 (ET-1), and vasoconstriction. We determined whether, during CH, depolarization-driven activation of L-type Ca2+ channels contributes to 1) maintenance of resting intracellular Ca2+ concentration ([Ca2+]i), 2) increased [Ca2+]i in response to ET-1 (10-8 M), and 3) ET-1-induced contraction. Using indo 1 microfluorescence, we determined that resting [Ca2+]i in PASMCs from intrapulmonary arteries of rats exposed to 10% O2 for 21 days was 293.9 ± 25.2 nM (vs. 153.6 ± 28.7 nM in normoxia). Resting [Ca2+]i was decreased after extracellular Ca2+ removal but not with nifedipine (10-6 M), an L-type Ca2+ channel antagonist. After CH, the ET-1-induced increase in [Ca2+]i was reduced and was abolished after extracellular Ca2+ removal or nifedipine. Removal of extracellular Ca2+ reduced ET-1-induced tension; however, nifedipine had only a slight effect. These data indicate that maintenance of resting [Ca2+]i in PASMCs from chronically hypoxic rats does not require activation of L-type Ca2+ channels and suggest that ET-1-induced contraction occurs by a mechanism primarily independent of changes in [Ca2+]i.

intracellular calcium concentration; endothelin-1; chronic hypoxia; pulmonary hypertension; contraction; voltage-gated calcium channels; smooth muscle; pulmonary artery smooth muscle cells


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