Abstract
The equilibrium between vasoconstrictors and vasodilators, as well as mitogenic and anti-mitogenic factors originating from the endothelium, is upset in certain situations and as a final result leads to an increase in pulmonary arterial pressure. The endothelial dysfunction is promoted by stimulants such as hypoxia, acidosis, free radicals, inflammatory mediators, tangential pressure caused by an increase in pulmonary blood flow from the left to the right by an intra-cardiac short circuit and fibrin derived from embolisms. Endothelial dysfunction and vascular remodelling are two important processes that explain the development of pulmonary hypertension. The therapeutic approach to this condition has progressed rapidly in the last few years, but there is still no ideal treatment. Future strategies could include improvements in the methods for administering the medications available, combinations of these, new therapeutic groups, and the possibility of gene therapy.
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