2
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Association of Hypertension and Obesity with Risk Factors of Cardiovascular Diseases in Children Aged 6–9 Years Old in the Eastern Cape Province of South Africa

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Cardiovascular disease (CVD) risk factors are known to begin early in life, but limited data on the relationship of obesity and hypertension with other known CVD risk factors, such as endothelial dysfunction, oxidative stress, and chronic low-grade inflammation is available on children. In this cross-sectional study involving 6–9 years old school children aged from the Eastern Cape Province of South Africa the relationship between obesity/hypertension and other risk factors for CVDs was investigated. General anthropometric parameters were measured, followed by blood pressure (BP) measurements and pulse wave velocity (PWV). Urine samples were collected for the determination of albumin, creatinine, asymmetric dimethylarginine (ADMA), 8-hydroxy-2deoxyguanosine (8-OHdG), and thiobarbituric acid-reactive substance (TBARS). Overweight/obesity (19.28%) and pre-hypertension/hypertension (42.16%) were prevalent in children. Mid-upper arm circumference (MUAC), a marker of obesity, was positively correlated with ADMA, while ADMA and PWV were significantly different ( p < 0.05) between hypertensive and normotensive children. Also, TBARS and 8-OHdG were significantly ( p < 0.05) increased in hypertensive subjects. Creatinine was significantly ( p < 0.05) increased in obese, as well as in hypertensive children, and positively associated with waist circumference (WC) and neck circumference (NC). In conclusion, obesity and hypertension were associated with renal-cardiovascular disease risk, while oxidative stress showed a possible association with obesity in 6 to 9 year old South African children of African descent. This suggests that South African children of African descent may be becoming more prone to developing CVDs, and therefore may require early intervention for the prevention of CVDs in the near future.

          Related collections

          Most cited references37

          • Record: found
          • Abstract: found
          • Article: not found

          The pathophysiology of hypertension in patients with obesity.

          The combination of obesity and hypertension is associated with high morbidity and mortality because it leads to cardiovascular and kidney disease. Potential mechanisms linking obesity to hypertension include dietary factors, metabolic, endothelial and vascular dysfunction, neuroendocrine imbalances, sodium retention, glomerular hyperfiltration, proteinuria, and maladaptive immune and inflammatory responses. Visceral adipose tissue also becomes resistant to insulin and leptin and is the site of altered secretion of molecules and hormones such as adiponectin, leptin, resistin, TNF and IL-6, which exacerbate obesity-associated cardiovascular disease. Accumulating evidence also suggests that the gut microbiome is important for modulating these mechanisms. Uric acid and altered incretin or dipeptidyl peptidase 4 activity further contribute to the development of hypertension in obesity. The pathophysiology of obesity-related hypertension is especially relevant to premenopausal women with obesity and type 2 diabetes mellitus who are at high risk of developing arterial stiffness and endothelial dysfunction. In this Review we discuss the relationship between obesity and hypertension with special emphasis on potential mechanisms and therapeutic targeting that might be used in a clinical setting.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Oxidative stress and endothelial dysfunction in hypertension.

            Systemic arterial hypertension is a highly prevalent cardiovascular risk factor that causes significant morbidity and mortality, and is becoming an increasingly common health problem because of the increasing longevity and prevalence of predisposing factors such as sedentary lifestyle, obesity and nutritional habits. Further complicating the impact of this disease, mild and moderate hypertension are usually asymptomatic, and their presence (and the subsequent increase in cardiovascular risk) is often unrecognized. The pathophysiology of hypertension involves a complex interaction of multiple vascular effectors including the activation of the sympathetic nervous system, of the renin-angiotensin-aldosterone system and of the inflammatory mediators. Subsequent vasoconstriction and inflammation ensue, leading to vessel wall remodeling and, finally, to the formation of atherosclerotic lesions as the hallmark of advanced disease. Oxidative stress and endothelial dysfunction are consistently observed in hypertensive subjects, but emerging evidence suggests that they also have a causal role in the molecular processes leading to hypertension. Reactive oxygen species (ROS) may directly alter vascular function or cause changes in vascular tone by several mechanisms including altered nitric oxide (NO) bioavailability or signaling. ROS-producing enzymes involved in the increased vascular oxidative stress observed during hypertension include the NADPH oxidase, xanthine oxidase, the mitochondrial respiratory chain and an uncoupled endothelial NO synthase. In the current review, we will summarize our current understanding of the molecular mechanisms in the development of hypertension with an emphasis on oxidative stress and endothelial dysfunction.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Arginase: a critical regulator of nitric oxide synthesis and vascular function.

              1. Arginase is the focal enzyme of the urea cycle hydrolysing L-arginine to urea and L-ornithine. Emerging studies have identified arginase in the vasculature and have implicated this enzyme in the regulation of nitric oxide (NO) synthesis and the development of vascular disease. 2. Arginase inhibits the production of NO via several potential mechanisms, including competition with NO synthase (NOS) for the substrate L-arginine, uncoupling of NOS resulting in the generation of the NO scavenger, superoxide and peroxynitrite, repression of the translation and stability of inducible NOS protein, inhibition of inducible NOS activity via the generation of urea and by sensitization of NOS to its endogenous inhibitor asymmetric dimethyl-L-arginine. 3. Upregulation of arginase inhibits endothelial NOS-mediated NO synthesis and may contribute to endothelial dysfunction in hypertension, ageing, ischaemia-reperfusion and diabetes. 4. Arginase also redirects the metabolism of L-arginine to L-ornithine and the formation of polyamines and L-proline, which are essential for smooth muscle cell growth and collagen synthesis. Therefore, the induction of arginase may also promote aberrant vessel wall remodelling and neointima formation. 5. Arginase represents a promising novel therapeutic target that may reverse endothelial and smooth muscle cell dysfunction and prevent vascular disease.
                Bookmark

                Author and article information

                Journal
                Children (Basel)
                Children (Basel)
                children
                Children
                MDPI
                2227-9067
                28 March 2020
                April 2020
                : 7
                : 4
                : 25
                Affiliations
                [1 ]Department of Human Biology, Faculty of Health Sciences, Walter Sisulu University PBX1, Mthatha 5117, South Africa; engoakoana@ 123456gmail.com (E.N.M.); bpletswalo@ 123456gmail.com (P.B.L.); mmungamba@ 123456gmail.com (M.M.M.); crusike@ 123456wsu.ac.za (C.R.S.-R.)
                [2 ]Department of Biological and Environmental Sciences, Faculty of Natural Sciences, Walter Sisulu University PBX1, Mthatha 5117, South Africa; gengwa@ 123456wsu.ac.za
                Author notes
                Article
                children-07-00025
                10.3390/children7040025
                7230217
                32231008
                01ba2f8f-9d22-4a6c-b011-882fb2e94621
                © 2020 by the authors.

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                : 29 January 2020
                : 11 March 2020
                Categories
                Article

                hypertension,obesity,oxidative stress,cardiovascular disease,endothelial dysfunction,renal dysfunction

                Comments

                Comment on this article