Renal xanthine oxidoreductase activity during development of hypertension in spontaneously hypertensive rats

Laakso, Juha; Teräväinen, Terttu-Liisa; Martelin, Eeva; Vaskonen, Timo; Lapatto, Risto

doi:10.1097/01.hjh.0000125441.28861.9f

Cited by 50 publications

(45 citation statements)

References 36 publications

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“…Antihypertensive effect Lack of antihypertensive effect Apocynin Prevented/attenuated mineralocorticoid-induced hypertension [86,240] Prevented/reversed glucocorticoid-induced hypertension [241] Prevented/reversed adrenocorticotropic hormone-induced hypertension [242] Prevented the development of Ang II-induced hypertension in mice [186] Prevented the development of renovascular hypertension [243] Prevented the development of hypertension induced by RAS activation [50] Reduced blood pressure in borderline and spontaneous hypertension [244] Attenuated salt-sensitive hypertension [245] Normalized blood pressure in a model of hypertension induced by disruption of dopamine D2 receptor [246] Failed to prevent the hypertension induced by chronic infusion of endothelin-1 [200] Failed to prevent hypertension in transgenic mice overexpressing renin or angiotensinogen [247,248] Failed to prevent Ang II-induced hypertension in rats [249,250] Gp91ds-tat Attenuated the blood pressure rise induced by Ang II in mice [209] Failed to attenuate salt-sensitive hypertension [251] Allopurinol Attenuated salt-sensitive hypertension [252] Prevented glucocorticoid-induced hypertension [253] Failed to prevent or attenuate mineralocorticoid-induced hypertension [254] Failed to prevent glucocorticoidinduced hypertension [255] Failed to prevent or attenuate adrenocorticotropic-induced hypertension [242] Failed to prevent the development of hypertension induced by the blockade of nitric oxide synthesis [256] Failed to prevent the progression of hypertension in young SHR [257] Oxypurinol Reduced blood pressure in SHR [258] Tempol Attenuated hypertension in SHR [201] Prevented the progression of hypertension in saltloaded SHRSP [259] Attenuated mineralocorticoid-induced hypertension [260] Failed to prevent Ang II-induced hypertension [264] Failed to attenuate hypertension induced by inhi...…”

Section: Drugmentioning

confidence: 99%

Lipid Peroxidation and Antioxidants in Arterial Hypertension

Sousa¹,

Afonso²,

Albino‐Teixeira³

et al. 2012

Lipid Peroxidation

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Section: Drugmentioning

confidence: 99%

Lipid Peroxidation and Antioxidants in Arterial Hypertension

Sousa¹,

Afonso²,

Albino‐Teixeira³

et al. 2012

Lipid Peroxidation

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“…21 In addition to effects on the vasculature, xanthine oxidase may have a function in end-organ damage in hypertension. 27 Mitochondria: Mitochondria are a major source and target of ROS. Some of the superoxide produced in the intermembrane space may be carried to the cytoplasm.…”

Section: Vascular Oxidative Stress and Hypertensionmentioning

confidence: 99%

“…[92][93][94][95][96] This situation can be explained by the hyperactivity of xanthine oxidase found in hypertension. 21,27 Exogenous antioxidants Vitamin C. Vitamin C is a potent water-soluble antioxidant. In the vascular wall, it functions as an enzyme modulator that upregulates eNOS and downregulates NADPH oxidase.…”

Section: Endogenous Antioxidantsmentioning

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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“…[1][2][3] One recent experimental study demonstrated that allopurinol, an xanthine oxidase inhibitor, prevented cardiac hypertrophy in rats with negligible effects on blood pressure (BP). 4 In humans, an elevated blood level of UA was reportedly associated with left ventricular hypertrophy (LVH) in hypertensive patients. 5,6 However, the hypertensive state may have confounded or modified the association because it could be related to both LVH and the UA level.…”

mentioning

confidence: 99%

Uric Acid and Left Ventricular Hypertrophy in Japanese Men

Mitsuhashi

Yatsuya

Matsushita

et al. 2009

Circ J

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Circ J 2009; 73: 667 -672 ric acid (UA) is produced in the terminal stage of purine metabolism catalyzed by xanthine oxidase, and is a primary cause of gout. The relationship between serum UA and cardiovascular diseases has been, however, controversial. [1][2][3] One recent experimental study demonstrated that allopurinol, an xanthine oxidase inhibitor, prevented cardiac hypertrophy in rats with negligible effects on blood pressure (BP). 4 In humans, an elevated blood level of UA was reportedly associated with left ventricular hypertrophy (LVH) in hypertensive patients. 5,6 However, the hypertensive state may have confounded or modified the association because it could be related to both LVH and the UA level. 7 In addition, because some antihypertensive drugs are reported to reduce LVH 8 or to affect the UA level, 5 assessing the association only in those not on hypertensive medication was warranted to clarify the role of UA as an independent risk factor for LVH. Editorial p 624The prevalence of LVH has been reported as approximately 20% in adult Japanese men. 9 LVH diagnosed by electrocardiography (ECG-LVH), as well as that diagnosed by echocardiography, is known to increase the risk of cardiovascular morbidity and mortality. [10][11][12] Although a major determinant of LVH is elevated BP, a previous report has indicated LVH in approximately 10% of the normotensive population. 13 Thus, studies to find other risk factors are warranted.In the present study, we investigated the association between UA and LVH in subjects not taking medication for hypertension (HTN). Moreover, we also investigated the association by stratifying subjects by BP, which might modify the association. Methods Study PopulationThis study used baseline data collected in 2002 for a workers' cohort study on cardiovascular diseases in Aichi, Japan. The questionnaires were returned from 7,991 people, of whom 6,651 (83.2%) expressed their written consent to the use of the information. Consent for the use of data obtained during their annual health examination and to donate residual blood samples used for the examination was obtained from 5,596 (70.0%) and 4,213 (52.7%) people, respectively. In this analysis, we first restricted the subjects to men with available information on weight, height, BP, ECG, UA and other biomarker concentrations (3,773 men), because of the small number of women with (Received July 3, 2008; revised manuscript received October 24, 2008; accepted December 3, 2008; released online February 19, 2009 Uric Acid and Left Ventricular Hypertrophy in Japanese MenHirotsugu Mitsuhashi, MD* , **; Hiroshi Yatsuya, MD*; Kunihiro Matsushita, MD* , **; Huiming Zhang, MD*; Rei Otsuka, PhD* , † ; Takashi Muramatsu, MD* , **; Seiko Takefuji, MD* , † † ;Yo Hotta, MD* , † † ; Takahisa Kondo, MD**; Toyoaki Murohara, MD**; Hideaki Toyoshima, MD* , ‡ ; Koji Tamakoshi, MD* , ‡ ‡ Background: Experimental studies have reported that allopurinol protects hypertensive rats from left ventricular hypertrophy (LVH) with negligible effects on blood ...

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Renal xanthine oxidoreductase activity during development of hypertension in spontaneously hypertensive rats

Cited by 50 publications

References 36 publications

Lipid Peroxidation and Antioxidants in Arterial Hypertension

Lipid Peroxidation and Antioxidants in Arterial Hypertension

The role of oxidative stress in the pathophysiology of hypertension

Uric Acid and Left Ventricular Hypertrophy in Japanese Men

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