We have hypothesized that in some patients with orthostatic intolerance a basal and stimulated enhancement of neurol symp0athetic traffic is present and results in a syndrom characterized by orthostatic tachycardia, blood pressure lability, elevated levels of plasma norepinephrine and pre-syncopal symptoms. To prove that a primary central hyperadrenergic disorder causes orthostatic intolerance we propose that several criteria must be met. First, there must be evidence of enhanced central sympathetic outflow, and this evidence should be supported by documentation of raised sympathetic noradrenergic activity based on biochemical physiological and pharmacological data. Second, there should be appropriately down-regulated A1 and b-adrenergic receptor sensitivity. Third, therapeutic reduction in sympathetic activity in affected patients should improve their symptoms and hemodynamic abnormalities. This proposal attempts to define the first line of evidence with studies manipulating central cardiovascular control such as mental stress, barbiturates administration and study of sympathetic function during sleep.
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