Increasing altitude is accompanied by decreased oxygen concentration. Studies on altitude natives and on sojourners at altitude have revealed the physiological and biological adaptations to short-term and long-term residency at high altitude that ensure adequate oxygen supply to tissues. Notable changes include altered ventilation rates, increased red blood cell number, and increased capillary volume. In recent years, the role of the autonomic nervous system in adaptation to altitude hypoxia has become apparent (181). Acute altitude exposure is associated with sympathetic activation and skin vasoconstriction. There is a blunted hypoxic pulmonary vasoconstriction response during the initial days of altitude exposure that has been shown to be independent of the NO/cyclic GMP pathway (182). Chronic hypobaric hypoxia increases sympathetic activation and causes contraction of vascular smooth muscle leading to a rise in pressure in the pulmonary arterial circulation, and remodeling of the pulmonary vasculature and pulmonary hypertension (183,184). Persistence of increased sympathetic activity and raised NA levels may account for the downreg-ulation of adrenergic receptors after prolonged high-altitude exposure (185,186). This may explain the decreased maximal heart rate in altitude acclimatized subjects. Elevated plasma NPY and adrenaline levels can be attributed to an effect of chronic hypoxia on the adrenal gland rather than an overactive sympathetic nervous system (187). During chronic hypoxia there is decreased myocardial NA uptake by the NA transporter, an event that precedes cardiac hypertrophy (188).
Studies at altitude have relevance in clinical situations at sea level. Tissue hy-poxia is a feature of many diseases, such as asthma, emphysema, coronary artery disease, and cancer. Knowledge of compensatory autonomic mechanisms to hypoxia may be harnessed to alleviate the symptoms of pathogenic hypoxia.
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