Role of oxidative stress in elevated blood pressure induced by high free fatty acids

Wang, Hui; Li, Hongliang; Hou, Zhiqiang; Lin, Pei; Shen, Xiaoxia; Li, Guangwei

doi:10.1038/hr.2008.35

Cited by 24 publications

(17 citation statements)

References 48 publications

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“…Most studies have linked fat and oxidative stress 44–46 . Animal and human fat have been shown to increase free radical production 47, 48 . This contributes to increased oxidative stress in the vascular wall, endothelial dysfunction and hypertension 49 .…”

Section: Discussionmentioning

confidence: 99%

Race/ethnicity determines the relationships between oxidative stress markers and blood pressure in individuals with high cardiovascular disease risk

et al. 2016

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Oxidative stress (OS) and cardiovascular (CV) reactivity are related to CV morbidity and mortality. However, little is known about the relationships between these CV risk factors and their confounders. We hypothesize that higher OS is linked to higher blood pressure (BP) reactivity to acute laboratory stressors and in the natural setting. We studied 137 subjects with a family history of hypertension and early myocardial infarction. There were 63 European Americans (EA’s) (38 males) and 74 African Americans (AA’s) (35 males), aged 19 to 36(27.6+/−3.1). The protocol included a competitive video game, cold stressor, and ambulatory BP recording. Blood samples were drawn 6 times for OS markers (8-OHdG and 8-Isoprostane) assay. Repeated measures analyses of covariance were used to test for mean differences and Pearson correlations were used to test OS and BP associations. There were no significant race/ethnicity differences in BP reactivity to either stressor (both p’s>0.48). 8-OHdG levels were significantly lower across all time points for AA’s than for EA’s (p<0.05) while levels of 8-isoprostane did not differ significantly (p>.10). Averaged 8-OHdG levels significantly correlated with SBP reactivity (r=0.45, <0.01) and 24-hour, daytime, and nighttime SBP (r range=0.37 to 0.42, all p’s<0.02) for EA’s but not for AA’s, whereas 8-isoprostane levels were significantly correlated with reactive SBP and nighttime DBP (both r’s=0.38, p<0.01) for AA’s but not for EA’s. These findings suggest a link between OS and BP changes in subjects at high risk for CV disease. Further, race/ethnicity determines which OS marker will impact BP variation implying race/ethnicity differences in OS related mechanisms of CVD.

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Section: Discussionmentioning

confidence: 99%

Race/ethnicity determines the relationships between oxidative stress markers and blood pressure in individuals with high cardiovascular disease risk

et al. 2016

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“…Experimental studies have confirmed that hypertension is related to oxidative stress, which could contribute to endothelial dysfunction, leading to elevated BP. 22 Further studies are needed to evaluate the mechanism of this association.…”

Section: Serum Ferritin Tibc and 4-year Incidence Of Hypertensionmentioning

confidence: 97%

Increased serum ferritin predicts the development of hypertension among middle-aged men

Kim

Baek

Song

et al. 2012

American Journal of Hypertension

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“…Potential adverse metabolic consequences of lipotoxicity (55) include abnormalities of glucose and lipid metabolism (5,56), and high blood pressure (57).…”

Section: Free Fatty Acids and Lipotoxicitymentioning

confidence: 99%

Adiposopathy

Bays¹

2011

Journal of the American College of Cardiology

360

153

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Being overweight or obese is a worldwide epidemic. Adiposity can cause fat mass-related cardiovascular disease (CVD). Adiposity may also cause adipocyte and adipose tissue anatomic and functional abnormalities, termed adiposopathy (adipose-opathy) or "sick fat," that result in endocrine and immune derangements. Adiposopathy may directly contribute to CVD through pericardiac and perivascular effects on the myocardium and blood vessels. Adiposopathy may also indirectly contribute to CVD through promoting or worsening major CVD risk factors such as type 2 diabetes mellitus, high blood pressure, and dyslipidemia. Despite CVD being the most common cause of mortality among overweight individuals, the pathophysiologic relationship between adiposity and CVD is often thought mysterious, as evidenced by "obesity paradoxes." Underlying this uncertainty are suggestions that excessive body fat does not always increase the risk of CVD and, in some cases, may actually decrease such risks. These paradoxical findings are made less paradoxical when the pathogenic potential of excessive body fat is assessed based on adipose tissue dysfunction rather than simply on increased fat mass alone. This introductory review 1) provides a brief historical perspective of the pathogenic potential of adipose tissue; 2) describes the relationships between adipose tissue (histology, embryology, and adipogenesis) and cardiovascular medicine; 3) outlines the anatomic, functional, endocrine, and immune manifestations of adiposopathy; and 4) describes the importance of cross talk and/or interactions of adipose tissue with other body tissues. Finally, this review describes how "sick fat" helps account for various clinical obesity/cardiovascular paradoxes, supporting adiposopathy as a cardiovascular disease.

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Role of oxidative stress in elevated blood pressure induced by high free fatty acids

Cited by 24 publications

References 48 publications

Race/ethnicity determines the relationships between oxidative stress markers and blood pressure in individuals with high cardiovascular disease risk

Race/ethnicity determines the relationships between oxidative stress markers and blood pressure in individuals with high cardiovascular disease risk

Increased serum ferritin predicts the development of hypertension among middle-aged men

Adiposopathy

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