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(Hypertension. 2002;39:173.)
© 2002 American Heart Association, Inc.

Scientific Contributions

Increased Sympathetic Activation in Idiopathic Orthostatic Intolerance

Role of Systemic Adrenoreceptor Sensitivity

Jens Jordan; John R. Shannon; Andre Diedrich; Bonnie K. Black; David Robertson

From the Clinical Research Center, Franz Volhard Clinic (J.J.), Charité, Berlin, Germany; and Nathan Blaser Shy-Drager Research Program, Autonomic Dysfunction Center, Vanderbilt University (J.R.S., A.D., B.K.B., D.R.), Nashville, Tenn.

Correspondence to Jens Jordan, MD, Clinical Research Center, Franz-Volhard-Clinic, Humboldt University, Wiltbergstr 50, 13125 Berlin, Germany. E-mail jordan{at}fvk-berlin.de

Idiopathic orthostatic intolerance (OI) is characterized by adrenergic symptoms with standing. Changes in central sympathetic tone or in adrenoreceptor sensitivity could contribute to this syndrome. In OI patients and control subjects, we determined heart rate (HR) and systolic blood pressure (SBP) changes after incremental bolus doses of isoproterenol and phenylephrine before and during ganglionic blockade with trimethaphan. SBP decreased by 17±1.6 mm Hg in patients and 3.9±3.8 mm Hg in control subjects (P<0.01) with trimethaphan. Patients with a larger decrease (28±3.8 mm Hg, n=7) in SBP with trimethaphan had greater supine SBP and supine and upright plasma norepinephrine levels than did patients with a lesser decrease (3.0±3.0 mm Hg, n=7) in SBP. Supine and orthostatic HRs were similar for the groups. The majority of patients had a normal HR response to isoproterenol before and during ganglionic blockade. Phenylephrine increased SBP similarly in patients and control subjects before and during blockade. Sympathetic support is increased in a subgroup of OI patients. Hyperadrenergic and nonhyperadrenergic subgroups have similar degrees of orthostatic tachycardia. Our findings suggest that the hyperadrenergic features of OI cannot be completely explained by systemic hypersensitivity of postsynaptic ₁- and ß-adrenoreceptors but rather originates in enhanced sympathetic activation.

Key Words: autonomic nervous system • tachycardia • postural tachycardia syndrome • receptors, adrenergic

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