LABORATORY STRESS IN NORMOTENSIVES, BORDERLINE HYPERTENSIVES AND ESSENTIAL HYPERTENSIVES IS ASSOCIATED WITH PRIMING OF PHAGOCYTIC-CELLS

Citation
S. Kopprasch et al., LABORATORY STRESS IN NORMOTENSIVES, BORDERLINE HYPERTENSIVES AND ESSENTIAL HYPERTENSIVES IS ASSOCIATED WITH PRIMING OF PHAGOCYTIC-CELLS, Stress medicine, 12(1), 1996, pp. 9-16
Citations number
37
Categorie Soggetti
Psychiatry,Psychiatry,Psychology
Journal title
ISSN journal
07488386
Volume
12
Issue
1
Year of publication
1996
Pages
9 - 16
Database
ISI
SICI code
0748-8386(1996)12:1<9:LSINBH>2.0.ZU;2-5
Abstract
The present study was designed to investigate the effect of standardiz ed laboratory physical and mental stress on phagocytic generation of r eactive oxygen species (ROS) and hormonal responses in normotensives ( NT), borderline hypertensives (BH) and essential hypertensives (EH). B H were characterized by increased neurohormonal activation in the pres tress situation as indicated by significant higher noradrenaline and A CTH values. Although physical stress resulted in a marked activation o f the sympatho-adrenal system in all groups, the BH group revealed a s trong tendency of more pronounced sympatho-adrenal response. The intra cellular and extracellular production of ROS was quantified using chem iluminescence (CL) assays. Phagocytic cells of NT, BH and EH responded to stress with a significantly enhanced zymosan-stimulated luminol- a nd lucigenin-amplified CL, predominantly localized intracellularly. In the BH group, but not in NT and EH, significant stress-related increa ses of extracellularly and intracellularly generated oxidative metabol ites of isolated granulocytes after stimulation with the chemotactic p eptide FMLP were found. Baseline values of all measured CL parameters did not differ between NT, BH and EH. The results show that stress is followed by priming of phagocytes for enhanced oxygen radical generati on. In addition to stress-related activation of intracellular ROS prod uction granulocytes of BH showed enhanced release of oxygen metabolite s into the extracellular space.