The effects of chronic hypoxia on the pharmacological responsiveness of the pulmonary artery

Chronic hypoxia (CH) is associated with several cardiopulmonary disorders. In vitro and in vivo studies have established the morphological changes, but yielded conflicting results about the functional changes induced by CH in the pulmonary vascular bed. CH increases the responsiveness to endothelium-dependent vasodilators in perfused lungs; however, in artery rings, a reduction is found in endothelium-dependent vasodilation. In CH, vasoconstriction induced by endothelin-l is enhanced and vasodilation produced by atrial natriuretic peptide and Kf channel openers is increased. Vasoconstriction produced by acute hypoxia can be either enhanced or reduced by CH, depending on the experimental protocol. An understanding of the functional changes associated with CH is particularly important for a rational approach to the treatment of disorders associated with CH.