In:
American Journal of Physiology-Lung Cellular and Molecular Physiology, American Physiological Society, Vol. 279, No. 5 ( 2000-11-01), p. L884-L894
Abstract:
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 Ca 2+ channels contributes to 1) maintenance of resting intracellular Ca 2+ concentration ([Ca 2+ ] i ), 2) increased [Ca 2+ ] i in response to ET-1 (10 −8 M), and 3) ET-1-induced contraction. Using indo 1 microfluorescence, we determined that resting [Ca 2+ ] i in PASMCs from intrapulmonary arteries of rats exposed to 10% O 2 for 21 days was 293.9 ± 25.2 nM (vs. 153.6 ± 28.7 nM in normoxia). Resting [Ca 2+ ] i was decreased after extracellular Ca 2+ removal but not with nifedipine (10 −6 M), an L-type Ca 2+ channel antagonist. After CH, the ET-1-induced increase in [Ca 2+ ] i was reduced and was abolished after extracellular Ca 2+ removal or nifedipine. Removal of extracellular Ca 2+ reduced ET-1-induced tension; however, nifedipine had only a slight effect. These data indicate that maintenance of resting [Ca 2+ ] i in PASMCs from chronically hypoxic rats does not require activation of L-type Ca 2+ channels and suggest that ET-1-induced contraction occurs by a mechanism primarily independent of changes in [Ca 2+ ] i .
Type of Medium:
Online Resource
ISSN:
1040-0605
,
1522-1504
DOI:
10.1152/ajplung.2000.279.5.L884
Language:
English
Publisher:
American Physiological Society
Publication Date:
2000
detail.hit.zdb_id:
1477300-4
SSG:
12
