article · African Journal of Clinical Medicine and Pharmacy Research
Hypertension in young adults is linked to oxidative stress, inflammation, and metabolic changes. A case-control study of 170 hypertensive and normotensive participants evaluated clinical features alongside biochemical markers. Hypertensive participants demonstrated significantly higher blood pressure, body weight, and body mass index compared to normotensive controls. Hypertensive individuals also had markedly lower levels of heme oxygenase-1, indicating reduced antioxidant capacity, as well as lower nitric oxide concentrations, which reflects impaired endothelial function. In contrast, vascular endothelial growth factor, insulin, iron, and adenosine deaminase levels were significantly higher in the hypertensive cohort. Correlation tests found no significant associations between heme oxygenase-1 and adenosine, adenosine deaminase, or xanthine oxidase. Overall, the findings define a distinct biochemical profile in young adults with high blood pressure, characterised by compromised vascular regulation, metabolic disturbance, and heightened inflammatory and oxidative stress markers.
High blood pressure among young adults involves complex metabolic and vascular disruptions that are not yet fully understood. Identifying specific biological markers, such as reduced antioxidant enzymes and altered vascular regulators, clarifies the physiological changes occurring in early-onset hypertension. This provides a clearer basis for researchers studying how oxidative stress and metabolic imbalance contribute to early cardiovascular risks.
This work represents early-stage observational research that identifies biochemical markers associated with young-adult hypertension. The findings could inform future diagnostic panel development or drug discovery efforts focused on antioxidant and vascular pathways, relevant to clinical diagnostics developers and pharmaceutical researchers. However, because the study is an observational case-control assessment that does not establish causality, any potential clinical or commercial application remains at a very early, pre-validation stage.
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Hypertension in young adults is increasingly recognized as a multifactorial condition associated with oxidative stress, inflammation, endothelial dysfunction, and metabolic imbalance. This study investigated the relationship between heme oxygenase-1 (HO-1) and hypertension among young adults, with particular attention to oxidative stress markers, inflammatory mediators, and metabolic profiles. A case–control study was conducted involving 170 hypertensive and normotensive participants. Sociodemographic and clinical characteristics were assessed alongside blood pressure, body mass index (BMI), body weight, and biochemical markers, including HO-1, vascular endothelial growth factor (VEGF), insulin, nitric oxide (NO), iron, and adenosine deaminase (ADA). Compared with normotensive controls, hypertensive participants had significantly higher systolic and diastolic blood pressure (p < 0.05), as well as higher BMI and body weight. HO-1 concentrations were markedly lower in hypertensive participants (p < 0.00001), indicating reduced antioxidant capacity. Conversely, VEGF concentrations were significantly elevated (p < 0.00001), consistent with altered vascular regulation. Hypertensive participants also exhibited increased insulin concentrations (p < 0.01), reduced NO concentrations (p < 0.00001), and elevated iron and ADA concentrations (p < 0.00001), collectively reflecting metabolic dysregulation, impaired endothelial function, oxidative stress, and inflammatory activity. Correlation analysis revealed no significant associations between HO-1 and adenosine, ADA, or xanthine oxidase (p > 0.05). These findings identify a distinct biochemical profile of young-adult hypertension characterized by reduced HO-1 and NO concentrations alongside increased VEGF, insulin, iron, and ADA concentrations. Although the case–control design does not establish causality, the results highlight HO-1 as a relevant component of the oxidative and vascular alterations associated with hypertension and support further longitudinal and mechanistic investigation.
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DOI: 10.58578/ajcmpr.v3i3.11826
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