Sympathetic Nervous System Activity in Major Depression: Basal and Desipramine-Induced Alterations in Plasma Norepinephrine Kinetics

doi:10.1001/archpsyc.1994.03950050071008

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Vol. 51 No. 5, May 1994

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Sympathetic Nervous System Activity in Major Depression

Basal and Desipramine-Induced Alterations in Plasma Norepinephrine Kinetics

Richard C. Veith, MD; Nancy Lewis, RN; Oscar A. Linares, MD; Robert F. Barnes, MD; Murray A. Raskind, MD; Enrique C. Villacres, MD; M. Michele Murburg, MD; E. Alexandra Ashleigh, MD; Sonia Castillo, PhD; Elaine R. Peskind, MD; Marcella Pascualy, MD; Jeffrey B. Halter, MD

Arch Gen Psychiatry. 1994;51(5):411-422.

Abstract

Background
To determine whether elevations of plasma norepinephrine (NE)in major depression represent increased sympathetic nervoussystem (SNS) activity and to assess the effects of desipraminehydrochloride on sympathetic function.

Methods
SNS activity was assessed in depressed patients and controlsby an isotope-dilution, plasma NE Kinetic technique using mathematicalmodeling and compartmental analysis. This approach providedestimates of the rate of NE appearance into an extravascularcompartment, which is the site of endogenous NE release fromSNS nerves, the corresponding rate of NE appearance into plasma,and the rate of NE clearance from plasma.

Results
Norepinephrine appearance into the extravascular and vascularcompartments was significantly elevated in 17 depressed patientscompared with that in 36 controls. The rate of NE clearancefrom plasma was similar in both groups. This is compatible withincreased SNS activity in major depression. Desipramine, givenfor 2 days, significantly reduced the concentration of NE inplasma of patients and controls by markedly suppressing therates of extravascular and vascular NE appearance, compatiblewith a short-term reduction in SNS activity. Desipramine prolongedthe rate of NE clearance from plasma, consistent with a blockadeof NE re-uptake into SNS nerve terminals. The initial suppressionof SNS activity by desipramine was reversed by long-term (28days) treatment of patients, with extravascular and vascularNE appearance rates returning to approximately basal levels.An associated rise in plasma NE concentrations compared withthe baseline was attributable to a progressive reduction inplasma NE clearance.

Conclusion
Sympathetic nervous system activity is elevated in major depressionand is suppressed by short-term desipramine administration.The demonstration of SNS reactivation occurring with prolongeddesipramine treatment is compatible with the theory that long-termtreatment desensitizes CNS ${alpha}$ ₂-adrenergic receptors and emphasizesthe value of examining the temporal course of responses to pharmacologicalchallenges of neuroendocrine systems. Previously reported elevationsof plasma NE during prolonged administration of tricyclic antidepressantsare probably the result of a reduction in plasma NE clearance,not an increase in SNS activity.

Author Affiliations

From the Geriatric Research, Education, and Clinical Center (GRECC) (Drs Veith, Raskind, and Castillo and Ms Lewis) and Psychiatry Service (Drs Barnes, Villacres, Murburg, Ashleigh, Peskind, and Pascualy), Seattle (Wash) VAMC; the Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle (Drs Veith, Raskind, Barnes, Villacres, Murburg, Ashleigh, Peskind, and Pascualy); GRECC, Ann Arbor (Mich) VAMC (Drs Linares and Halter); and the Division of Geriatric Medicine, Department of Internal Medicine, University of Michigan, Ann Arbor (Drs Linares and Halter).

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