| Several recent studies provide evidence that exposure to chronic
hypoxia (CH) markedly increases basal vascular smooth muscle (VSM) intracellular Ca2+ ([Ca2+]i) and alters
[Ca2+]i handling pathways in pulmonary VSM and endothelial cells. Considering that elevated VSM [Ca2+]i
has been implicated in mediating the enhanced vasoconstrictor and remodeling responses to CH induced
pulmonary hypertension, it is important to understand the components involved in the regulation of VSM
[Ca2+]i. Recent studies demonstrate that store-operated Ca2+ entry (SOCE) in pulmonary VSM is upregulated
following CH. The novelty of the present study is that we will characterize a unique class of ion channels,
acid sensing ion channels (ASICs), in mediating SOCE. We will further determine whether ASICs contribute
to the elevated resting [Ca2+]i and increased SOCE observed following CH. |
