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Sympathetic Nervous System Activation and Vascular Endothelial Function With Chronic Hypoxia.

Exposure to high altitude with lower inspired oxygen levels evokes an array of acute and chronic changes that allow newcomers to mountainous regions of the world to recreate, work, and even live successfully up to altitudes of 4000 meters.1 Cardiac output acutely increases to maintain tissue oxygen delivery followed by slower nongenomic responses (eg, a progressive rise in ventilation over hours and days). Ultimately, altered gene transcription by HIF (hypoxia-inducible factor) leads to erythropoietindriven red cell production and changes in intermediary metabolism that enhance oxygen utilization efficiency. The sympathetic nervous system (SNS) through direct innervation and adrenal activation regulates key responses including increasing cardiac output through augmenting heart rate and myocardial contractility and opposing the hypoxia-induced systemic vasodilation.2 In the short term of minutes to hours, the SNS-response to hypoxia resembles the evolutionary flight or fight response that ensures survival in situations of acute stress. With unabating or frequent intermittent stress as occurs with prolonged hypoxic exposure, the consequences of sustained SNS activation become unproductive and harmful. One of these is an increase in systemic vascular resistance leading to hypertension, which is a problem for those remaining at high altitude and in some populations with generational histories in the mountains.