Journals of Gerontology Series A: Biological Sciences and Medical Sciences Large Type Edition
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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 55:M155-M159 (2000)
© 2000 The Gerontological Society of America

Increased Plasma Norepinephrine Response to Yohimbine in Elderly Men

Eric C. Petrieb,d, Elaine R. Peskinda,b,d, Dorcas J. Dobiea,b,d, Richard C. Veithc,d and Murray A. Raskinda,b,d

a Veterans Affairs Northwest Network Mental Illness Research, Education and Clinical Center
b Mental Health Service
c Geriatric Research, Education and Clinical Center (GRECC)
d Department of Psychiatry and Behavioral Sciences, University of Washington School of Medicine, Seattle, Washington

Eric C. Petrie, Veterans Affairs Puget Sound Health Care System, Mental Health Service (S-116), 1660 S. Columbian Way, Seattle, WA 98108 E-mail: petrie.eric{at}seattle.va.gov.

Background. The effects of aging on sympathetic nervous system and adrenomedullary outflow were estimated by the measurement of plasma norepinephrine (NE) and epinephrine (EPI) responses to yohimbine and clonidine in healthy young and healthy older subjects.

Methods. Yohimbine (0.65 mg/kg), clonidine (5 µg/kg), and placebo were administered on separate days in random order to 5 healthy older men (age 74 ± 1 years) and 18 healthy young men (age 26 ± 1 years). NE and EPI were measured by radioenzymatic assay in plasma samples obtained before and 30, 60, and 90 minutes after drug administration.

Results. Plasma NE increases after yohimbine were greater in older men than in young men, but plasma NE decreases following clonidine did not differ between groups. Plasma NE and systolic blood pressure were higher in older men than in young men at baseline but no longer differed 90 minutes after clonidine. Plasma EPI increases after yohimbine and decreases after clonidine did not differ between groups.

Conclusions. These results suggest increased sympathetic nervous system outflow in human aging that is not a function of reduced responsiveness of alpha-2 adrenoreceptor-mediated feedback inhibition.






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