Premium
Ca 2 + Channels and Chronic Hypoxia
Author(s) -
SHIMODA LARISSA A.,
WANG JIAN,
SYLVESTER J. T.
Publication year - 2006
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1080/10739680600930305
Subject(s) - hypoxia (environmental) , homeostasis , pulmonary hypertension , intracellular , lung , pathogenesis , vascular smooth muscle , biology , endocrinology , medicine , microbiology and biotechnology , immunology , chemistry , smooth muscle , oxygen , organic chemistry
Many chronic lung diseases are associated with prolonged exposure to alveolar hypoxia, resulting in the development of pulmonary hypertension. While the exact mechanisms underlying the pathogenesis of hypoxic pulmonary hypertension remain poorly understood, a key role for changes in Ca 2+ homeostasis has emerged. Intracellular Ca 2+ concentration controls a variety of pulmonary vascular cell functions, including contraction, gene expression, growth, barrier function and synthesis of vasoactive substances. Several studies indicate that prolonged exposure to hypoxia causes alterations in the expression and activity of several Ca 2+ handling pathways in pulmonary arterial smooth muscle cells. In contrast, the effect of chronic hypoxia on Ca 2+ homeostasis in pulmonary arterial endothelial cells is relatively unexplored. In this review, we discuss data from our laboratory and others describing the effects of prolonged hypoxia on pulmonary vascular smooth muscle and endothelial cell Ca 2+ homeostasis and the various Ca 2+ channels and handling pathways involved in these responses. We will also highlight future directions of investigation that might improve our understanding of the response of pulmonary vascular cells to chronic hypoxia.