EFFECTS OF BETA-ADRENERGIC-BLOCKADE ON IMMUNOLOGICAL AND CARDIOVASCULAR CHANGES INDUCED BY MENTAL STRESS

Citation
Rj. Benschop et al., EFFECTS OF BETA-ADRENERGIC-BLOCKADE ON IMMUNOLOGICAL AND CARDIOVASCULAR CHANGES INDUCED BY MENTAL STRESS, Circulation, 89(2), 1994, pp. 762-769
Citations number
42
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
89
Issue
2
Year of publication
1994
Pages
762 - 769
Database
ISI
SICI code
0009-7322(1994)89:2<762:EOBOIA>2.0.ZU;2-B
Abstract
Background Acute mental stress evokes responses in the cardiovascular and the immune systems. In particular, the subset of natural killer (N K) cells is found to be responsive to mental stress. The role of beta- adrenergic mechanisms in these processes is the subject of this invest igation. Methods and Results Healthy male volunteers (n=31) were subje cted to two consecutive mental tasks. Subjects were randomly assigned to a beta-blocker (propranolol 40 mg) or a placebo group. The capsules were ingested 1 hour before the tasks. The tasks evoked sympathetic r esponses, as indicated by an increase in heart rate and a decrease in the preejection period. These effects were abolished under beta-blocka de, indicating that effective beta-blockade was achieved. In the immun e system, significant increases were found for the number of NK cells and NK cell activity in the placebo group; these increases were absent in the propranolol group. In addition, an increase in all lymphocyte subsets was observed in subjects who had ingested propranolol. This in crease, however, was also observed in subjects who had received propra nolol but had not performed the tasks, indicating that these non-subse t-specific increases in lymphocytes were a side effect of the beta-blo cker. Conclusions Mental stress induces activation of the sympathetic nervous system, with concomitant increases in the number of NK cells i n the circulation. These changes were inhibited by propranolol, indica ting that stress-induced increases in the number and activity of NK ce lls in the circulation are controlled by a beta-adrenergic mechanism.