Plasma xanthine oxidase activity is related to increased sodium and left ventricular hypertrophy in resistant hypertension

Butts, Brittany; Calhoun, David A.; Denney, Thomas S.; Lloyd, Steven G.; Gupta, Himanshu; Gaddam, Krishna K.; Aban, Inmaculada; Oparil, Suzanne; Sanders, Paul W.; Patel, Rakesh P.; Collawn, James F.; Dell’Italia, Louis J.

doi:10.1016/j.freeradbiomed.2019.01.029

Cited by 16 publications

(21 citation statements)

References 47 publications

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“…Angiotensin II can induce XO levels in aortic endothelial cells in vitro (Landmesser et al, 2007), which may be relevant in CVD states. For example, in patients with coronary artery disease, XO is activated along with NOX (Spiekermann et al, 2003), and plasma XO levels are associated with left ventricular hypertrophy in hypertension (Butts et al, 2019). Assuming that XO activation is a causal mechanism in disease, one might expect that UA would correlate with disease or disease severity.…”

Section: Ros Generators and Toxifiers In Diseasementioning

confidence: 99%

On the Clinical Pharmacology of Reactive Oxygen Species

Casas

Nogales

Mucke

et al. 2020

Pharmacological Reviews

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Section: Ros Generators and Toxifiers In Diseasementioning

confidence: 99%

On the Clinical Pharmacology of Reactive Oxygen Species

Casas

Nogales

Mucke

et al. 2020

Pharmacological Reviews

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“…In addition to mitochondria and NOX, ROS in endothelial cells are also generated by xanthine oxidase and neutrophils, especially at the stage of I/R injury [69]. Xanthine oxidase, the conversion product of oxidative damage to xanthine dehydrogenase, produces superoxide and hydrogen peroxide during purine metabolism [70,71]. This process is more prominent in endothelial cells [72].…”

Section: Mitochondrial Oxidative Stressmentioning

confidence: 99%

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

Zhou

Toan

2020

Biomolecules

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Mitochondria are key regulators of cell fate through controlling ATP generation and releasing pro-apoptotic factors. Cardiac ischemia/reperfusion (I/R) injury to the coronary microcirculation has manifestations ranging in severity from reversible edema to interstitial hemorrhage. A number of mechanisms have been proposed to explain the cardiac microvascular I/R injury including edema, impaired vasomotion, coronary microembolization, and capillary destruction. In contrast to their role in cell types with higher energy demands, mitochondria in endothelial cells primarily function in signaling cellular responses to environmental cues. It is clear that abnormal mitochondrial signatures, including mitochondrial oxidative stress, mitochondrial fission, mitochondrial fusion, and mitophagy, play a substantial role in endothelial cell function. While the pathogenic role of each of these mitochondrial alterations in the endothelial cells I/R injury remains complex, profiling of mitochondrial oxidative stress and mitochondrial dynamics in endothelial cell dysfunction may offer promising potential targets in the search for novel diagnostics and therapeutics in cardiac microvascular I/R injury. The objective of this review is to discuss the role of mitochondrial oxidative stress on cardiac microvascular endothelial cells dysfunction. Mitochondrial dynamics, including mitochondrial fission and fusion, are critically discussed to understand their roles in endothelial cell survival. Finally, mitophagy, as a degradative mechanism for damaged mitochondria, is summarized to figure out its contribution to the progression of microvascular I/R injury.

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“…These results indicated that vascular protective property of sUA is likely to be detected, especially in hemodialysis patients demonstrating reduced oxidative stress and uniform good nutrition status. [35,36], xanthine oxidase activity and production of ROS would differ among patients without XOIs. Moreover, these patients without XOIs appeared to exhibit various nutrition status.…”

Section: Discussionmentioning

confidence: 99%

Relationship between serum uric acid level and vascular injury markers in hemodialysis patients

et al. 2020

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Purpose It has been reported that hyperuricemia causes vascular endothelial injury. Most hemodialysis patients present with hyperuricemia and also with vascular injury, resulting in cardiovascular diseases (CVD). However, the association of serum uric acid (sUA) with vascular injury markers in hemodialysis patients remains unclear. This study aimed to investigate this and discuss the mechanism by which uric acid causes vascular injury. Methods We enrolled 48 Japanese maintenance hemodialysis patients without any history of CVD. The association between sUA level and three vascular injury markers (reactive hyperemia index [RHI], ankle-brachial index [ABI], and cardio ankle vascular index [CAVI]) was investigated by linear-and logistic regression analyses. Results The median natural logarithm RHI (LnRHI) was 0.36. Linear regression analysis revealed a significant positive correlation between sUA level and LnRHI (β = 0.42, p = 0.001) in all patients. Moreover, a significant, strongly positive correlation was observed between sUA and LnRHI in patients who were treated with xanthine oxidase inhibitors (XOIs) (β = 0.75, p = 0.001). Further, the linear analysis showed a significant negative correlation between sUA level and CAVI in patients who were treated with XOIs (β = − 0.52, p = 0.049). sUA level was not significantly associated with ABI abnormality. Conclusions It is possible that a high level of sUA is significantly associated with better vascular endothelial function and condition of vascular tone in hemodialysis patients who were treated with XOIs. The findings suggest a significant paradox between sUA level and vascular endothelial function in hemodialysis patients; however, the opposite has been reported in patients without hemodialysis.

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Plasma xanthine oxidase activity is related to increased sodium and left ventricular hypertrophy in resistant hypertension

Cited by 16 publications

References 47 publications

On the Clinical Pharmacology of Reactive Oxygen Species

On the Clinical Pharmacology of Reactive Oxygen Species

Pathological Roles of Mitochondrial Oxidative Stress and Mitochondrial Dynamics in Cardiac Microvascular Ischemia/Reperfusion Injury

Relationship between serum uric acid level and vascular injury markers in hemodialysis patients

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