Abstract

People of Black African ethnicity (BA) have greater prevalence of hypertension compared with those of White European ethnicity (WE) and are at greater risk of developing hypertension‐associated cardiovascular disease (CVD). Older WE non‐dipper hypertensives show endothelial dysfunction. Endothelial dysfunction and higher prevalence of non‐dipping nocturnal blood pressure have been documented in Blacks relative to Whites. Novel environmental stress stimuli evoke sympathetic vasoconstriction in renal and splanchnic vasculature, but vasodilatation in limb muscle, which may habituate on repetition. In young adults altered response to novel stimuli is predictive of developing hypertension later on in life. However, It is not known whether non‐dippers also show endothelial dysfunction and altered responses to environmental stressors. Thus, we hypothesized that non dippers would show smaller muscle vasodilator or muscle vasoconstrictive responses on repetition of an environmental stressor and blunted reactive hyperaemia relative to dippers. Experiments were performed on 17 WEs (21±0.64 years) and 16 BAs (22±0.77 years) who were resident in the UK. Responses were recorded following release of arterial occlusion for 2 min (reactive hyperaemia) and by 5 sound stimuli (S1–5; 100 dB, 2 KHz). Continuous arterial blood pressure (ABP) was recorded by finger photoplethysmography. Forearm blood flow (FBF) was recorded by venous occlusion plethysmography; forearm vascular conductance (FVC) was calculated as FBF/ABP. 24 hour Ambulatory blood pressure monitoring was done. Relative to WES, BAs showed higher 24 hour systolic blood pressure (SBP)(110±1.33 vs 117±3.17 mmHg) and higher sleep‐time SBP (99±1.36 vs 108±3.05 mmHg) p<0.05 as well as higher proportion of pre‐/hypertensives (7/16, 40%) compared with WE (1,5.8%). 40% BAs were non‐ dippers compared to 17.6 % WE. Six of the pre‐/hypertensive BAs were nocturnal dippers. Relative to normotensive BA dippers, BA non‐dippers showed higher sleep SBP (93±4.65 vs 108±3.01 mmHg) and heart rate (59±4.69 vs 72±3.11 bpm) p<0.05. Relative to WE dippers, the WE non dippers showed higher day‐time and night time mean ABP (85.25±1.14 vs 91.57±2.39 mmHg) ; (71.55±0.88 vs 81.25±1.71 mmHg) p<0.05. During reactive hyperaemia, there was no difference between dippers and non‐dippers in the two ethnic groups ( WE: +0.39± 0.03 vs +0.45± 0.08; BA : +0.41± 0.05 vs +0.34± 0.05 p>0.05 ). During S1–5, WE and BA dippers showed a net increase in FVC indicating forearm vasodilatation (WE, +0.005±0.002 CU; BA, +0.007±0.002 CU) whilst WE and BA non‐dippers showed a net decrease in FVC indicating forearm vasoconstriction, (WE − 0.007±0.004 CU; BA −0.007±0.003 CU). These results indicate that in young normotensive non‐dippers, sympathetic vasoconstriction to mental stress precedes development of endothelial dysfunction and could serve as an early indicator of cardiovascular disorder. Thus, we propose that exaggerated sympathetic vasoconstrictor response to environmental stressors contributes to the development of hypertension and CVD in non‐dippersThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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