title: Nocturnal blood pressure dipping in the hypertension of autonomic failure.
abstract: Blood pressure (BP) normally decreases during the night. Absence of this phenomenon (nondipping) is associated with increased cardiovascular risk. Altered autonomic and endocrine circadian rhythms are suspected to play a role. Patients with peripheral autonomic failure offer a unique opportunity to study this phenomenon, because approximately 50% develop supine hypertension despite very low autonomic function. The purpose of this study was to define the prevalence of dipping in these patients and to determine whether dipping is associated with less severe autonomic impairment or exaggerated nocturnal sodium excretion. We collected BP and urine from 8:00 pm to 8:00 am in 41 peripheral autonomic failure patients with supine hypertension. Dipping (systolic BP fall >or=10% during 12 am to 6 am from baseline [8 pm to 10 pm]) occurred in 34% of patients, with an average decrease of -44+/-4 mm Hg at 4 am. Systolic BP, averaged from 12 am to 6 am, decreased to normotensive levels in 50% (n=7) of dippers and 15% (n=7) of nondippers. There were no significant differences in the severity of autonomic failure, nocturnal diuresis, or natriuresis (0.18+/-0.01 in dippers versus 0.18+/-0.01 mEq/mg of creatinine in nondippers; P=0.522) between groups. At 8:00 am, orthostatic hypotension was similar between groups (-84/-35+/-9/4 mm Hg in dippers versus -93/-39+/-6/3 mm Hg in nondippers; P=0.356 for systolic BP). In conclusion, dipping was observed in one third of patients with peripheral autonomic failure, so that a significant percentage of patients would not require treatment for supine hypertension. Dipping was not associated with increased nocturnal urinary sodium or volume excretion or less severe autonomic failure. Thus, mechanisms independent of autonomic pathways contribute to BP dipping in these patients.
authors.affiliation: Division of Clinical Pharmacology and Department of Medicine, Vanderbilt University School of Medicine, Nashville, TN, USA.
authors.forename: Luis E
authors.initials: LE
authors.lastname: Okamoto
authors.forename: Alfredo
authors.initials: A
authors.lastname: Gamboa
authors.forename: Cyndya
authors.initials: C
authors.lastname: Shibao
authors.forename: Bonnie K
authors.initials: BK
authors.lastname: Black
authors.forename: André
authors.initials: A
authors.lastname: Diedrich
authors.forename: Satish R
authors.initials: SR
authors.lastname: Raj
authors.forename: David
authors.initials: D
authors.lastname: Robertson
authors.forename: Italo
authors.initials: I
authors.lastname: Biaggioni
mesh_terms: D000368:Aged; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001794:Blood Pressure / Q000502:physiology*; D002940:Circadian Rhythm / Q000502:physiology*; D003404:Creatinine / Q000652:urine; D005260:Female; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology* / Q000652:urine; D008297:Male; D005996:Nitroglycerin / Q000627:therapeutic use; D012964:Sodium / Q000652:urine; D014665:Vasodilator Agents / Q000627:therapeutic use
chemical_list: D014665:Vasodilator Agents; D012964:Sodium; D003404:Creatinine; D005996:Nitroglycerin