Supine
hypertension occurs commonly in primary chronic autonomic failure. This study explored whether supine
hypertension in this setting is associated with
orthostatic hypotension (
OH), and if so, what mechanisms might underlie this association. Supine and upright blood pressures, hemodynamic responses to the Valsalva maneuver, baroreflex-cardiovagal gain, and plasma
norepinephrine (NE) levels were measured in
pure autonomic failure (PAF),
multiple-system atrophy (MSA) with or without
OH, and
Parkinson's disease (PD) with or without
OH. Controls included age-matched, healthy volunteers and patients with
essential hypertension or those referred for
dysautonomia. Baroreflex-cardiovagal gain was calculated from the relation between the interbeat interval and systolic pressure during the Valsalva maneuver. PAF, MSA with
OH, and PD with
OH all featured supine
hypertension, which was equivalent in severity to that in
essential hypertension, regardless of
fludrocortisone treatment. Among patients with PD or MSA, those with
OH had higher mean arterial pressure during supine rest (109+/-3 mm Hg) than did those lacking
OH (96+/-3 mm Hg, P=0.002). Baroreflex-cardiovagal gain and orthostatic increments in plasma NE levels were markedly decreased in all 3 groups with
OH. Among patients with PD or MSA, those with
OH had much lower mean baroreflex-cardiovagal gain (0.74+/-0.10 ms/mm Hg) than did those lacking
OH (3.13+/-0.72 ms/mm Hg, P=0.0002). In chronic autonomic failure, supine
hypertension is linked to both
OH and low baroreflex-cardiovagal gain [corrected]. The finding of lower plasma NE levels in patients with than without supine
hypertension suggests involvement of pressor mechanisms independent of the sympathetic nervous system.