Abstract
Nitric oxide (NO) is a simple molecule causing vasodilation. It is synthesized endoge- nously by a number of cell types including the vascular endothelium.
In contrast to the systemic vessels, where a continuous NO production contributes significantly to the ba- sal tone regulation, resting NO synthesis is minimal in a healthy pulmonary circulation. However, it increases during acute pulmonary vasoconstriction and during chronic pul- monary hypertension, most likely as a feedback mechanism against excessive elevations of intravascular pressure.