Both endothelium-dependent dilatation responses and muscle vasodilator responses to environmental stressors are impaired in young Black Africans and may contribute to their predisposition to develop hypertension

eople of Black African ethnicity (BA) have greater prevalence of hypertension than those of White European ethnicity and greater risk of developing hypertension-associated cardiovascular disease (CVD). Exaggerated sympathetic responses to environmental stressors in young adult life is associated with subsequent development of hypertension and young, normotensive BAs showed exaggerated increases in muscle sympathetic nerve activity to mental arithmetic relative to WEs. Novel environmental stress stimuli evoke sympathetic vasoconstriction in renal and splanchnic vasculature, but vasodilatation in limb muscle, which habituates on repetition. Further, in young adults with hypertensive parents, the muscle vasodilatation is blunted or even reversed to vasoconstriction. Thus, we hypothesized that young BAs would show greater pressor responses, smaller muscle vasodilator responses and/or less habituation on repetition of an environmental stressor than WEs. Since the muscle vasodilator response is partly dependent on endothelium dependent dilators we hypothesized that reactive hyperaemia is blunted in BAs. Experiments were performed on young BAs (18–26 years; n=8) and WEs (19–22; n=16), who were resident in the UK. Responses were recorded following release of arterial occlusion for 2min (reactive hyperaemia) and by 5 sound stimuli (S1–5; 100dB, 2KHz, for 30s each at randomized intervals of 5–10min). Arterial blood pressure (ABP) was recorded by finger photoplethysmography. Forearm blood flow (FBF) was recorded at intervals by venous occlusion plethysmography; forearm vascular conductance (FVC) was calculated as FBF/ABP. Reactive hyperaemia was larger in WEs than BAs, peak change in FVC was +0.44±0.038 vs +0.34±0.13 conductance units, CU; P<0.05). During S1, WEs and BAs showed a net increase in FVC indicating forearm vasodilatation, the change in FVC at 15s being +0.021±0.013 vs +0.08±0.01CU. However, at 15s into S2–5, WEs consistently showed a net increase in FVC, whereas BAs show a net decrease, the changes in FVC at 15s in S5 being +0.029±0.01 and −0.056±0.051 CU respectively (P=0.05, WE vs BA S1–S5). Concomitantly, resting mean ABP was similar in WEs and BAs (88±3 vs 83±3mmHg) and showed no net change in response to sound in WEs (−4.4±2.2 and −1.2±3.0mmHg at 15s in S1 and S5 respectively), but a consistent increase in BAs (+3.8±0.6 and 10.4±1.0mmHg at 15s in S1 and S5). These results indicate that even in young BAs, the muscle vasodilatation induced by environmental stressors habituates and reverses to vasoconstriction more readily than young WEs, so contributing to the more pronounced pressor response in BAs. Reactive hyperaemia, which is at least partly endothelium-dependent, was also blunted in young BAs. Thus, we propose that impaired endothelial dilatation coupled with exaggerated sympathetic vasoconstrictor responses to environmental stressors contribute to the development of hypertension and CVD in BAs.