ABSTRACT
The pulmonary vasculature is a low-pressure, high-capacitance vascular bed that uniquely reacts to changes in O2 tension in the perfusate. Unlike systemic arteries, which generally dilate in response to reduced Po2, pulmonary arterial vessels constrict when the oxygen tension falls below a threshold of 55mmHg (1). The so-called hypoxic pulmonary vasoconstriction (HPV) has an absolute requirement for Ca2þ mobilization from the extracellular space and involves membrane depolarization of the pulmonary arterial smooth muscle cells. Until recently, our understanding of the ionic mechanisms acting not only in HPV but also in chronic hypoxia-induced alterations in pulmonary vasomotor tone and in primary and secondary forms of pulmonary hypertension was very limited.
