The ability of NO inhalation toimprove pulmonary hemodynamics and quality of life in selected patients withpulmonary hypertension [53] further suggests the importance of relative NO deficiency in this disorder.Collectively these and other studies indicate that post-translationalalterations in eNOS regulation and/or enhanced NO degradation rather thanreduced eNOS expression contribute significantly to pulmonary hypertensionpathogenesis [38, 44, 46, 47]. This evidence concerns the gene NOS3 and hypertensive disorder.