Abstract
A loss of arterial elasticity increases the risk for cardiovascular events. Oxidative injury to the vessel wall may be one of the underlying mechanisms influencing arterial elasticity. We compared markers of oxidative stress, antioxidant capacity, inflammation, windkessel compliance (Cwk), and total peripheral resistance (TPR) in black and white South Africans. Associations of arterial compliance and vascular resistance (as indicated by TPR) with oxidative stress, antioxidant capacity and inflammatory markers were also investigated. We included 146 black and 181 white men and women. Measurements from the Finometer device were used to calculate Cwk and TPR while thiobarbituric acids reactive substances (TBARS), glutathione peroxidase (GPx), C-reactive protein (CRP), and interleukin-6 (IL-6) were analyzed in serum or urine samples. Black participants had higher TPR, TBARS, GPx, CRP, and IL-6 levels (all p ≤ 0.018) and lower Cwk (both p ≤ 0.013) compared to white participants. Multiple regression analyses revealed independent associations of Cwk (β = −0.27, p = 0.015) and TPR (β = 0.18, p = 0.018) with TBARS in black participants, while Cwk (β = −0.10; p = 0.019) and TPR (β = 0.13, p = 0.047) were independently associated with GPx in white participants. Decreased arterial compliance and increased vascular resistance associated with increased oxidative damage independent of hypertensive status in black participants. These results suggest that oxidative stress plays a role in early vascular changes in a black population prone to the development of cardiovascular disease.
Acknowledgements
The Sympathetic Activity and Ambulatory Blood Pressure in Africans (SABPA) study would not have been possible without the voluntary collaboration of the participants and the Department of Education, North West Province, South Africa. We gratefully acknowledge the technical assistance of Mrs. Tina Scholtz, Dr.Szabolcs Péter, and Sr Chrissie Lessing. Any opinion, findings and conclusions or recommendations expressed in this material are those of the authors and therefore the National Research Foundation does not accept any liability in regard thereto.
Disclosure statement
The authors declare no conflict of interest.
Funding statement
This work was supported by the National Research Foundation [80643], the Medical Research Council, the North-West University (Potchefstroom, South-Africa), the Metabolic Syndrome Institute (France) and Roche Products Pty Ltd (South-Africa).