During the 5 years, 24% of Africans with optimal BP developed hypertension. The surge in hypertension in Africa is largely explained by modifiable risk factors. Public health strategies should focus aggressively on lifestyle to prevent a catastrophic burden on the national health system.

A defensive pathway revealed disturbed vascular function showing dissociation between behavioural and physiological ß-adrenergic active coping responses in Africans. Vascular responsiveness facilitated silent ischaemia events and structural LVH changes which potentially explain the increased risk for incident ischaemic stroke in black Africans.

Objective: Concentrations of adiponectin, an adipocytokine with insulin-sensitizing actions, may vary according to ethnic group. This study aimed to determine whether fasting adiponectin levels of Caucasian and African women differ. A second objective was to determine which components of the metabolic syndrome are more closely related to adiponectinemia in both groups. Design: A cross-sectional study including 102 urban African and 115 Caucasian women with a wide range of obesity aged 20-55 years. Methods: Anthropometric measurements were taken, namely weight, height, body mass index, waist circumference, and hip circumference. Cardiovascular measurements included blood pressure and arterial compliance. Fasting blood samples were taken to determine glucose, insulin, C-peptide, leptin, adiponectin, and lipid levels. Results: Mean adiponectin levels of the whole groups did not differ, but normal weight African women (NZ38) showed marginally lower adiponectin levels than their Caucasian counterparts (NZ41; PZ0.047). No differences in adiponectin were shown for overweight and obese women. Separate multiple regression analyses for ethnic groups showed that only homeostasis model assessment-insulin resistance (HOMA-IR) significantly contributed to the variance in adiponectin levels of African women, whereas leptin, triacylglycerol levels and HOMA-IR contributed significantly to adiponectin variance in Caucasian women. An additional multiple regression analysis in a combined ethnic group (NZ217) showed ethnicity to be a significant contributor to variances in adiponectin levels. Conclusions: Even though adiponectin levels of these ethnic groups are similar, different associations of adiponectin with leptin and triacylglycerol levels might indicate that there are ethnic differences regarding the mechanistic functions of adiponectin within the scope of the metabolic syndrome.

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Objective: Alarming increases in hypertension and type 2 diabetes among Africans accentuate the need to identify factors that could serve as targets for prevention or treatment. In Caucasian populations, asymmetric dimethylarginine (ADMA), the predominant endogenous nitric oxide synthase inhibitor, is associated with cardiovascular disease and insulin resistance (IR). ADMA's counterpart, symmetric dimethylarginine (SDMA), originally thought to be inert, was recently also linked with cardiovascular risk. Since little information regarding ADMA or SDMA is available for Africans, our aim was to explore the relationships of ADMA and SDMA with measures of arterial stiffness and IR in Africans and Caucasians from South Africa. Methods: The study consisted of 235 nonsmoking, nondiabetic, nonobese, human immunodeficiency virus-uninfected Africans (nZ64) and Caucasians (nZ171), aged 20-70 years. We measured blood pressure, pulse wave velocity, ADMA, SDMA, and IR (homeostasis model assessment, HOMA). Results: African and Caucasian men had similar ADMA and SDMA, whereas Caucasian women had higher ADMA and SDMA than African women (P!0.05). African men and Caucasian women indicated strong correlations of ADMA with arterial stiffness (rZ0.47, PZ0.021; rZ0.26, PZ0.008), confirmed in multivariate analyses. Caucasian participants showed negative associations between SDMA and HOMA, being strongest in the men (rZK0.41; PZ0.002). Conclusion: Our results indicate that ADMA is independently associated with vascular dysfunction in African men and Caucasian women. A strong, independent negative association of SDMA with IR was found only in Caucasian participants. The molecular explanation for this is unclear, but these findings motivate experimental studies that could shed more light on these relationships.

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Background Psychobiological processes linking stress and vascular diseases remain poorly understood. The retina and the brain share a common embryonic-diencephalon origin and blood-barrier physiology e.g. ongoing ischemia facilitates S100B release with astrocytic activity and glial-fibrillary-acidic-protein expression (GFAP). However, GFAP decreases revealed astrocyte pathology in the prefrontal cortex of depression/suicide cases; and might be a key mechanism in stress – disease pathways. Methods A chronic emotional stress phenotype independent of age, ethnicity or sex was used to stratify the current prospective cohort (N ​= ​359; aged 46 ​± ​9 years) into Stress (N ​= ​236) and no-Stress groups (N ​= ​123). Prospective data for glia ischemia risk markers were obtained, including 24 ​h BP, fasting S100B, GFAP, HbA 1C and tumor-necrosis-factor-α (TNF-α). At 3-yr follow-up: diastolic-ocular-perfusion-pressure (indicating hypo-perfusion risk) was measured and retinal vessel calibers were quantified from digital images in the mydriatic eye. Results Higher hypertension (75% vs. 16%), diabetes (13% vs. 0%) and retinopathy (57% vs. 45%) prevalence was observed in Stress compared to no-Stress individuals. Stressed individuals had consistently raised S100B, TNF-α, HbA 1C and higher diastolic-ocular-perfusion-pressure, but decreases in GFAP and GFAP:S100B. Furthermore stroke risk markers, arterial narrowing and venous widening were associated with consistently raised S100B, GFAP:S100B (p ​= ​0.060), TNF-α and higher diastolic-ocular-perfusion-pressure [Adj. R 2 0.39–0.41, p ​≤ ​0.05]. No retinal-glia associations were evident in the no-Stress group. Conclusions Retinal-glia ischemia and inflammation was induced by chronic stress. Persistent higher inflammation and S100B with GFAP decreases further reflected stress-induced astrocyte pathology in the human retina. It is recommended to increase awareness on chronic stress and susceptibility for brain ischemia.

Whether renal mechanisms of hypertension primarily translate into increases in systemic vascular resistance (SVR) in all populations is uncertain. We determined whether renal mechanisms associate with either increases in SVR (and impedance to flow) or systemic flow in a community of African ancestry.Method: In a South African community sampled across the full adult age range (n ¼ 546), we assessed stroke volume (SV), peak aortic flow (Q), SVR, characteristic impedance (Zc) and total arterial compliance (TAC) from velocity and diameter measurements in the outflow tract (echocardiography) and central arterial pressures. Renal changes were determined from creatinine clearance (glomerular filtration rate, GFR) and fractional Na þ excretion (FeNa þ ) (derived from 24-h urine collections).Results: Independent of confounders (including MAP and pressures generated by the product of Q and Zc), SV (and hence cardiac output) (P < 0.0001) and Q (P < 0.01), but not SVR, Zc or TAC (P ¼ 0.09-0.20) were independently associated with decreases in both GFR (index of nephron number) and FeNa þ . Through an interactive effect (P < 0.0001), the impact of GFR on SV or Q was strongly determined by FeNa þ and vice versa. The relationship between the GFR-FeNa þ interaction and either SV or Q was noted in those above or below 50 years of age, although neither GFR, FeNa þ nor the interaction were independently associated with SVR, Zc or TAC at any age. Conclusion:Across the full adult lifespan, in groups of African ancestry, renal mechanisms of hypertension translate into increases in systemic flow rather than into resistance or impedance to flow.