期刊
HIGH ALTITUDE MEDICINE & BIOLOGY
卷 6, 期 2, 页码 133-146出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ham.2005.6.133
关键词
vascular smooth muscle; ion channels; proliferation; membrane potential; chronic hypoxia
资金
- NHLBI NIH HHS [R01 HL054043, HL 69753, HL 66941, HL 64945, R01 HL066012, R01 HL064945, HL 66012, P01 HL066941, R29 HL054043, U01 HL069758, HL 54043] Funding Source: Medline
Remillard, Carmelle V., and Jason X.-J. Yuan. High altitude pulmonary hypertension: role of K+ and Ca2+ channels. High Alt Med Biol 6:133-146, 2005.-Global alveolar hypoxia, as experienced at high-altitude living, has a serious impact on vascular physiology, particularly on the pulmonary vasculature. The effects of sustained hypoxia on pulmonary arteries include sustained vasoconstriction and enhanced medial hypertrophy. As the major component of the vascular media, pulmonary artery smooth muscle cells (PASMC) are the main effectors of the physiological response(s) induced during or following hypoxic exposure. Endothelial cells, on the other hand, can sense humoral and hemodynamic changes incurred by hypoxia, triggering their production of vasoactive and mitogenic factors that then alter PASMC function and growth. Transmembrane ion flux through channels in the plasma membrane not only modulates excitation-contraction coupling in PASMC, but also regulates cell volume, apoptosis, and proliferation. In this review, we examine the roles of K+ and Ca2+ channels in the pulmonary vasoconstriction and vascular remodeling observed during chronic hypoxia-induced pulmonary hypertension.
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