Abstract
After the discovery of the endogenous vasodilator, 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. However, numerous studies summarized in this review proved that, in reality, this simple scheme does not apply.
In pulmonary hypertension, NO synthesis increases. The rise in pulmonary artery pressure is partly blunted by this protective mechanism.