This study investigated the impact of stress on effectors of the L-arginine/nitric oxide (NO) system including the endogenous inhibitor asymmetric dimethylarginine (ADMA).
Black (n = 168) and white (n = 206) South African teachers were exposed to a mental and a physical stressor for 1 minute, respectively. Serum samples for determination of L-arginine, NO metabolites, ADMA, and symmetric dimethylarginine (SDMA) were obtained at rest and during stress exposure. Perception of task stressfulness was assessed on a 7-point Likert scale, and psychological distress was estimated by the General Health Questionnaire.
Black South Africans exhibited higher resting levels of NO metabolites (adjusted mean [standard error of the mean] = 11.3 [1.3] versus 3.9 [1.1] μmol/l, p < .001) but lower circulating ADMA (0.62 [0.02] versus 0.70 [0.02] μmol/l, p = .004) and SDMA (0.41 [0.01] versus 0.53 [0.01] μmol/l, p < .001) than did white South Africans. Ethnicity-by-psychological distress interaction was observed for resting levels of ADMA (p = .002), SDMA (p = .038), and L-arginine (p = .048). Ethnic differences in responses to experimental stress were evident for NO metabolites (blacks versus whites: 5.94 [1.55] versus −0.74 [1.25] μmol/l, p = .004) and SDMA (blacks versus whites: −0.02 [0.01] versus 0.02 [0.01] μmol/l, p = .004). Ethnicity-by-psychological distress interaction for stress responses was found for L-arginine/ADMA ratio (p = .027).
The L-arginine/NO system is affected by psychosocial distress with higher susceptibility in black South Africans. This interaction may contribute to the higher cardiovascular disease risk in black South Africans.
From the Autonomic and Neuroendocrinological Laboratory Dresden (M.R., T.Z.), Department of Neurology, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany; Department of Epidemiology and Public Health (M.H.), University College London, London, UK; Hypertension in Africa Research Team (N.T.M., L.M.), School for Physiology, Nutrition and Consumer Sciences, North-West University, Potchefstroom, South Africa; Neurovascular Hypertension & Kidney Disease (M.P.S.) and Human Neurotransmitters Laboratories (G.W.L.), Baker IDI Heart and Diabetes Institute, Melbourne, Australia; and Department of Experimental and Clinical Pharmacology and Toxicology (R.H.B.), University Medical Center-Hamburg Eppendorf, Hamburg, Germany.
Address correspondence and reprint requests to Manja Reimann, PhD, Autonomic and Neuroendocrinological Laboratory Dresden, Department of Neurology, University Hospital Carl Gustav Carus at the Dresden University of Technology, Fetscherstr. 74, 01307 Dresden, Germany. E-mail: firstname.lastname@example.org
Received for publication January 17, 2013; revision received June 14, 2013.