Conclusion
Both acute and chronic hypoxia alter resting [Ca 2+]i value and Ca 2+ transients in PASMCs. These alterations are related to hypoxia-mediated effects on various pathways implicated in PASMC Ca 2+ homeostasis: voltage-dependent and-independent Ca 2+ influx, IP 3 R 5 Ca 2+ re-uptake, etc. These alterations also play a role in both structural and reactivity changes of the pulmonary circulation in the course of the development of PAHT, as well as in its potential reversal upon normal air breathing. Further studies are therefore required to provide a comprehensive description of the variety of hypoxia-induced effects on calcium signaling in PASMCs, and to identify the common mechanism(s) leading to these various effects in order to define new molecular therapeutic targets.