Tempol or candesartan prevents high-fat diet-induced hypertension and renal damage in spontaneously hypertensive rats

Chung, Sungjin; Park, Cheol Whee; Shin, Seok Joon; Lim, Ji Hee; Chung, Hyun Wha; Youn, Dong-Ye; Kim, Hyung Wook; Kim, Byung Soo; Lee, Jeong-Hwa; Kim, Gheun-Ho; Chang, Yoon Sik

doi:10.1093/ndt/gfp472

Cited by 54 publications

(52 citation statements)

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“…However, it has been demonstrated that a HFD increased body weight, serum cholesterol, and BP in SHRs and the changes in metabolic parameters were associated with cardiovascular dysfunction in these animals (Šedová et al 2004(Šedová et al , Cao et al 2011. Chung et al (2010) have shown that after 12 weeks on the HFD, SHRs gained more body weight, their systolic BP was further elevated, and glucose intolerance induced, but there were no significant differences in the insulin resistance index, serum lipid profile, plasma renin activity, and serum aldosterone levels. On the other hand, Knight et al (2008) observed that HFD consumption for 10 weeks had no effect on systolic BP of SHRs.…”

Section: Rat Models Of Obesity and Hypertensionmentioning

confidence: 96%

Obesity-related hypertension: possible pathophysiological mechanisms

Vaněčková¹,

Maletı́nská²,

Behuliak³

et al. 2014

Journal of Endocrinology

130

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Hypertension is one of the major risk factors of cardiovascular diseases, but despite a century of clinical and basic research, the discrete etiology of this disease is still not fully understood. The same is true for obesity, which is recognized as a major global epidemic health problem nowadays. Obesity is associated with an increasing prevalence of the metabolic syndrome, a cluster of risk factors including hypertension, abdominal obesity, dyslipidemia, and hyperglycemia. Epidemiological studies have shown that excess weight gain predicts future development of hypertension, and the relationship between BMI and blood pressure (BP) appears to be almost linear in different populations. There is no doubt that obesity-related hypertension is a multifactorial and polygenic trait, and multiple potential pathogenetic mechanisms probably contribute to the development of higher BP in obese humans. These include hyperinsulinemia, activation of the renin-angiotensin-aldosterone system, sympathetic nervous system stimulation, abnormal levels of certain adipokines such as leptin, or cytokines acting at the vascular endothelial level. Moreover, some genetic and epigenetic mechanisms are also in play. Although the full manifestation of both hypertension and obesity occurs predominantly in adulthood, their roots can be traced back to early ontogeny. The detailed knowledge of alterations occurring in the organism of experimental animals during particular critical periods (developmental windows) could help to solve this phenomenon in humans and might facilitate the age-specific prevention of human obesity-related hypertension. In addition, better understanding of particular pathophysiological mechanisms might be useful in so-called personalized medicine. Key Words" obesity " hypertension " sympathetic nervous system " renin-angiotensin system " critical developmental periods " epigenetics " rat

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Section: Rat Models Of Obesity and Hypertensionmentioning

confidence: 96%

Obesity-related hypertension: possible pathophysiological mechanisms

Vaněčková¹,

Maletı́nská²,

Behuliak³

et al. 2014

Journal of Endocrinology

130

View full text Add to dashboard Cite

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“…53 There is evidence which suggests that a high-fat diet induces renal inflammation and aggravation of blood pressure via ROS in spontaneously hypertensive rats. 54 Additionally, metabolic syndrome is a risk factor for chronic kidney disease (CKD) that is at least in part independent of diabetes and hypertension and probably mediated by ROS. Moreover, the onset and maintenance of renal damage may worsen metabolic syndrome features, such as hypertension, leading to potential vicious cycles.…”

Section: Urotensin-iimentioning

confidence: 99%

The role of oxidative stress in the pathophysiology of hypertension

2011

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Hypertension is considered to be the most important risk factor in the development of cardiovascular disease. An increasing body of evidence suggests that oxidative stress, which results in an excessive generation of reactive oxygen species (ROS), has a key role in the pathogenesis of hypertension. The modulation of the vasomotor system involves ROS as mediators of vasoconstriction induced by angiotensin II, endothelin-1 and urotensin-II, among others. The bioavailability of nitric oxide (NO), which is a major vasodilator, is highly dependent on the redox status. Under physiological conditions, low concentrations of intracellular ROS have an important role in the normal redox signaling maintaining vascular function and integrity. However, under pathophysiological conditions, increased levels of ROS contribute to vascular dysfunction and remodeling through oxidative damage. In human hypertension, an increase in the production of superoxide anions and hydrogen peroxide, a decrease in NO synthesis and a reduction in antioxidant bioavailability have been observed. In turn, antioxidants are reducing agents that can neutralize these oxidative and otherwise damaging biomolecules. The use of antioxidant vitamins, such as vitamins C and E, has gained considerable interest as protecting agents against vascular endothelial damage. Available data support the role of these vitamins as effective antioxidants that can counteract ROS effects. This review discusses the mechanisms involved in ROS generation, the role of oxidative stress in the pathogenesis of vascular damage in hypertension, and the possible therapeutic strategies that could prevent or treat this disorder. Hypertension Research (2011) 34, 431-440; doi:10.1038/hr.2010.264; published online 13 January 2011Keywords: antioxidants; endothelial dysfunction; oxidative stress INTRODUCTION Hypertension is considered the most important risk factor for the occurrence of cardiovascular disease. 1 Oxidative stress has gained attention as one of the fundamental mechanisms responsible for the development of hypertension. Reactive oxygen species (ROS) have an important role in the homeostasis of the vascular wall; hence, they could be part of the mechanism that leads to hypertension. 2-4 Thus, increased ROS production, reduced nitric oxide (NO) levels and reduced antioxidant bioavailability were demonstrated in experimental and human hypertension. Vascular superoxide is primarily derived from nicotinamide adenine dineucleotide phosphate (NADPH) oxidase when stimulated by hormones, such as angiotensin II (AT-II), endothelin-1 (ET-1) and urotensin II. In addition, increased ROS production may be generated by mechanical stimuli on the vascular wall, which increase with hypertension. ROS-induced vasoconstriction results from increased intracellular calcium concentration, thereby contributing to the pathogenesis of hypertension. 2 Vasomotor tone is dependent on a delicate balance between vasoconstrictor and vasodilator forces that result from the interaction between the components of...

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“…42 For example, an upregulation of reactive oxygen species appeared to precede the development of hypertension, 43,44 and an antioxidant regimen arrested the process. 44,45 In vasculature, the major source of reactive oxygen species was from a family of non-phagocytic NAD(P)H oxidases, which comprised a catalytic core (Nox/p22 phox ) and several cytosolic subunits (p47 phox , p67 phox , p40 phox , Rac). 46 The core and the subunits heterodimerized in response to physiological and pathological stimulation such as angiotensin II (Ang II), 47 thereby facilitating superoxide (that is, O 2 À ) production.…”

Section: Molecular Targets Of Chlorogenic Acid In Blood-pressure Regumentioning

confidence: 99%

Antihypertensive effects and mechanisms of chlorogenic acids

et al. 2011

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Chlorogenic acids (CGAs) are potent antioxidants found in certain foods and drinks, most notably in coffee. In recent years, basic and clinical investigations have implied that the consumption of chlorogenic acid can have an anti-hypertension effect. Mechanistically, the metabolites of CGAs attenuate oxidative stress (reactive oxygen species), which leads to the benefit of blood-pressure reduction through improved endothelial function and nitric oxide bioavailability in the arterial vasculature. This review article highlights the physiological and biochemical findings on this subject and highlights some remaining issues that merit further scientific and clinical exploration. In the framework of lifestyle modification for the management of cardiovascular risk factors, the dietary consumption of CGAs may hold promise for providing a non-pharmacological approach for the prevention and treatment of high blood pressure.

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Tempol or candesartan prevents high-fat diet-induced hypertension and renal damage in spontaneously hypertensive rats

Cited by 54 publications

References 54 publications

Obesity-related hypertension: possible pathophysiological mechanisms

Obesity-related hypertension: possible pathophysiological mechanisms

The role of oxidative stress in the pathophysiology of hypertension

Antihypertensive effects and mechanisms of chlorogenic acids

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