BNP regulates basal endothelial tone through endothelial receptors via nitric oxide (Kone, 2001 Kuhn, 2012). Although BNP >100 picogram/ml indicates cardiac pathology because its release is related to cardiac tissue stretching, however, chronic hypoxia alone can raise BNP levels without any cardiac tissue stretching (Arjamaa and Aaltonen, 2012 Arjamaa and Nikinmaa, 2011). Elevated HIF1 alpha and sub clinical elevated BNP has been found to be associated with endothelial dysfunction while rise in BNP post hypoxia indicates microangipathy (Khatri et al., 2020). Our previous study showed reduced vascular compliance and fluid shift from extracellular to intracellular space during acute hypoxia was associated with reduced peripheral tissue oxygen consumption and nitric oxide level indicating endothelial dysfunction (Khatri et al., 2020).
The primary response of healthy cell to acute hypoxia is nitric oxide production and increased biogenesis. Subclinical pulmonary dysfunction, reduced HbA levels and systemic inflammation among HAPE-S were associated with endothelial dysfunction (Soree et al., 2016 Gupta et al., 2017 Mishra et al., 2016). Exaggerated increase in PVR to hypoxia is associated with elevated baseline HIF1α (Soree et al., 2016). Studies showed exaggerated PVR to hypoxia in HAPE-S while normal PVR observed in HAPE resistant individuals (Gupta et al., 2016 Dehnert et al., 2015). Increased pulmonary vascular response (PVR) to hypoxia have been shown by high altitude pulmonary edema susceptible (episode of high-altitude pulmonary edema in past, HAPE-S) and associated with elevated endothelin-1 at sea level and high altitude (Sartori et al., 1999). Endothelial dysfunction leading to subclinical vascular pathology at sea level can manifests as acute mountain sickness (AMS), high altitude pulmonary edema (HAPE), high altitude cerebral edema (HACE). Endothelial dysfunction reflects a specific atherogenic milieu, associated with perfusion abnormalities or cardiovascular events. Certain individuals despite several risk factors do not progress to atherosclerotic disease indicate healthy endothelial function while increased intra cellular oxidative stress has been considered as a major mechanism involved in pathogenesis of endothelial dysfunction. Role of traditional risk factors (life style diseases like - DM, HTN, COPD, Metabolic disorder etc) in development of atherosclerotic disease is well documented. Lifestyle diseases can be associated with reduced vascular compliance due to endothelial dysfunction.
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