Abstract
Introduction: Hypoxia, either from altitude or clinical ailments is associated with pathophysiological conditions like mountain sickness and/or hypoxia-induced pulmonary hypertension. An endothelial dysfunction plays a crucial role in the manifestation of these diseases. Asymmetric dimethylarginine (ADMA) is an endogenous formed NO synthase (NOS) inhibitor and well known as a risk factor for respiratory diseases associated with an endothelial dysfunction. ADMA is metabolized by dimethylarginine dimethylaminohydrolases (DDAH). Our study was aimed to assess the molecular involvement and behavior of the ADMA/NO pathway during chronic hypoxia (CH) and intermittent hypoxia (CIH).
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