title: Association between supine hypertension and orthostatic hypotension in autonomic failure.
abstract: 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.
authors.affiliation: the Clinical Neurocardiology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Md 20892-1620, USA. goldsteind@ninds.nih.gov
authors.forename: David S
authors.initials: DS
authors.lastname: Goldstein
authors.forename: Sandra
authors.initials: S
authors.lastname: Pechnik
authors.forename: Courtney
authors.initials: C
authors.lastname: Holmes
authors.forename: Basil
authors.initials: B
authors.lastname: Eldadah
authors.forename: Yehonatan
authors.initials: Y
authors.lastname: Sharabi
mesh_terms: D000368:Aged; D001342:Autonomic Nervous System Diseases / Q000150:complications* / Q000175:diagnosis / Q000503:physiopathology; D017704:Baroreflex; D001794:Blood Pressure; D005260:Female; D005438:Fludrocortisone / Q000627:therapeutic use; D006321:Heart / Q000294:innervation; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000188:drug therapy / Q000209:etiology; D007024:Hypotension, Orthostatic / Q000150:complications* / Q000175:diagnosis / Q000188:drug therapy; D007980:Levodopa / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D009638:Norepinephrine / Q000097:blood; D010300:Parkinson Disease / Q000150:complications / Q000188:drug therapy; D012189:Retrospective Studies; D016683:Supine Position; D013564:Sympathetic Nervous System / Q000503:physiopathology; D014630:Vagus Nerve / Q000503:physiopathology; D014636:Valsalva Maneuver
chemical_list: D007980:Levodopa; D005438:Fludrocortisone; D009638:Norepinephrine