One of the most important differences between the pulmonary and systemic circulation is a considerably lower blood pressure and hemodynamic resistance in the pulmonary circulation. After the discovery of the endogenous vasodilatator, nitric oxide (NO), it had been assumed that pulmonary vasculature is characterized by a high tonic NO production, which might contribute to the low basal tone of these vessels. Incapacity to maintain this high NO production would then lead to the development of pulmonary hypertension. However, numerous studies summarized in this review gradually proved that, in reality, this simple scheme does not apply. Healthy pulmonary vessels usually produce only relatively small amounts of NO. In pulmonary hypertension, NO synthesis increases. The rise in pulmonary artery pressure is partly blunted by this protective mechanism, at least until the pulmonary endothelium (a major source of NO) is damaged by the permanent and severe elevation of the intravascular pressure.

        Key words: pulmonary circulation, hypoxia, nitric oxide, regulation