Highlights on pulmonary hypertension: a commentary

Abstract

Physiological description of the pulmonary vascular response to hypoxia and to disease has clarified the func­ tion of pulmonary arteries. The understanding of the cellular regulation of vascular tone has proceeded at a rapid pace, with the discovery of endothelium-derived relaxing factor (EDRF) [11], and its identification as the gas nitric oxide (NO) [12]. Also, endothelin-1, a polypep­ tide elaborated by endothelium, has been found to be the most powerful natural vasoconstriction [13]. Production of endothelium-derived nitric oxide (EDNO) and endothelin1 are influenced by hypoxia. EDNO may be reduced in COLD [14], whilst endothelin-1 [15] can be increased by hypoxia. These observations not only provide insight into the possible role of endothelium in pulmonary hyper­ tension but have led to radically new treatments. Inhaled NO is a selective pulmonary vasodilator [16], and may have an important action in improving gas exchange in patients with acute respiratory distress syndrome (ARDS) [17]. Finally, the vascular smooth muscle cells of the pul­ monary arteries may be particularly important in deter­ mining hypoxic vasoconstriction [ 18]. The articles included in the series on Pulmonary Hypertension published in this and future issues of the Journal provide new insights into major areas of growth of knowledge in the pulmonary vasculature. For brevity, much has been omitted, particularly the description of the pulmonary vasculitides or the involvement of the blood vessels in systemic disease. These will, no doubt, be covered by future symposia; by which time, the struc­ tural and functional consequences of chronic hypoxia on pulmonary vas~ulature are likely to have been fully elu­ cidated.