(Circulation. 2000;101:2710.)
© 2000 American Heart Association, Inc.
Clinical Investigation and Reports |
Sympathetically Mediated Hypertension in Autonomic Failure
From the Autonomic Dysfunction Center, Vanderbilt University, Nashville Tenn (J.R.S., J.J., A.D., B.P., B.K.B., D.R., I.B.), and the Clinical Research Center, Franz Volhard Clinic, Berlin, Germany (J.J.).
Correspondence to Italo Biaggioni, MD, Autonomic Dysfunction Center, AA3228 MCN, Vanderbilt University, Nashville, TN 37232-2195. E-mail italo.biaggioni{at}mcmail.vanderbilt.edu
Background—Approximately 50% of patients with primary autonomic failure have supine hypertension. We investigated whether this supine hypertension could be driven by residual sympathetic activity.
Methods and Results—In patients with multiple system
atrophy (MSA) or pure autonomic failure (PAF), we studied the effect of
oral yohimbine on seated systolic blood pressure (SBP), the
effect of ganglionic blockade (with trimethaphan) on supine SBP and
plasma catecholamine levels, and the effect of
1-adrenoreceptor blockade
(phentolamine) on supine SBP. The SBP response to yohimbine was
greater in patients with MSA than in those with PAF (area under the
curve, 2248±543 versus 467±209 mm Hg · min;
P=0.022). MSA patients with a higher supine SBP had a
greater response than those with a lower supine SBP (3874±809 versus
785±189 mm Hg · min; P=0.0017); this
relationship was not seen in PAF patients. MSA patients had a marked
depressor response to low infusion rates of trimethaphan; the response
in PAF patients was more variable. Plasma
norepinephrine decreased in both groups, but heart rate did
not change in either group. At 1 mg/min, trimethaphan decreased
supine SBP by 67±8 and 12±6 mm Hg in MSA and PAF
patients, respectively (P<0.0001). Cardiac index and
total peripheral resistance decreased in MSA patients by
33.4±5.8% and 40.7±9.5%, respectively (P=0.0015).
Patients having a depressor response to trimethaphan also had a
depressor response to phentolamine. In MSA patients, the
pressor response to yohimbine and the decrease in SBP with 1 mg/min
trimethaphan were correlated (r=0.98;
P=0.001).
Conclusions—Residual sympathetic activity drives supine hypertension in MSA. It contributes to, but does not completely explain, supine hypertension in PAF.
Key Words: nervous system, autonomic • hypertension • trimethaphan • phentolamine • norepinephrine
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