Abstract
In their paper in the July 27 issue,1 Giaid and Saleh demonstrate reduced expression of endothelial nitric oxide synthase in the lungs of patients with pulmonary hypertension. Although these data are extremely provocative, we have several reservations about this study. First, the paper does not present a balanced view of the current literature on the role and expression of nitric oxide in normal lung and in pulmonary hypertension. For example, the authors state that “nitric oxide plays an important part in . . . maintaining low pressure in the normal pulmonary circuit.” This remains controversial. Nishiwaki et al.2 have demonstrated that nitric oxide is not important in controlling the low pulmonary vascular tone of conscious dogs, and we have demonstrated that in normal rats nitric oxide synthase is not expressed in small resistance vessels of the lung. There is also an evolving literature demonstrating that, in animal models of pulmonary hypertension, nitric oxide synthase is up-regulated rather than down-regulated.3,4