Abstract

CHINCHILLA, MANUEL et al. THE ROLE OF NITRIC OXIDE (NO) IN THE NORMAL PHYSIOLOGY OF THE AIRWAY AND ITS IMPLICATIONS ON THE PATHOPHYSIOLOGY OF PULMONARY HYPERTENSION. rev.fac.med [online]. 2008, vol.16, n.2, pp.215-225. ISSN 0121-5256.

Pulmonary hypertension is a disease of the pulmonary microvasculature characterized by vasoconstriction, smooth muscle and endothelial proliferation, and thrombosis. Many molecules have been implicated in the etiology, demonstrating an increased production of vasoconstrictor agents as well as mitogenic, prothrombotic and inflammatory mediators such as tromboxano A2, endothelin (ET), and the inhibitor of the plasminogen activator, together with a low production of vasodilator substances such as prostacyclin (PGI2) and nitric oxide (NO), which in physiological conditions, acts as a modulator of the basal tones of the pulmonary vessels, an inflammatory mediator, and an immunomodulator. The histopathology of the injuries in pulmonary hypertension, triggered by the alteration in the production or activity of NO, which is caused by an accumulation of free radicals that leads to lower bioavailability of NO, suggests that the damage in the endothelium and the proliferative stimulus are fundamental processes for their development. This article reviews the role played by NO in the normal physiology of the airway and its implications on the pathophysiology of pulmonary hypertension.

Keywords : hypertension pulmonary; nitric oxide; endothelin; epoprostenol; vascular endothelial.

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