Uric Acid and Hypertension: Cause or Effect?

Mazzali, Marilda; Kanbay, Mehmet; Segal, Mark S.; Shafiu, Mohamed; Jalal, Diana; Feig, Daniel I.; Johnson, Richard J.

doi:10.1007/s11926-010-0094-1

Cited by 126 publications

(96 citation statements)

References 99 publications

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“…90,91 However, there is evidence of a potential association between the plasma concentration of uric acid, blood pressure and cardiovascular risk. [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.…”

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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Section: Endogenous Antioxidantsmentioning

confidence: 99%

The role of oxidative stress in the pathophysiology of hypertension

2011

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“…3 One of the recently proposed risk factors for hypertension is hyperuricemia. 4 Observational studies have consistently confirmed the association between serum uric acid and incidence of hypertension. 5,6 However, high serum uric acid is associated with comorbidities, such as cardiovascular disease, kidney disease, or diabetes mellitus and antihypertensive medications, that can influence the association of serum uric acid and blood pressure.…”

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confidence: 94%

Association of Uric Acid Genetic Risk Score With Blood Pressure

et al. 2014

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Abstract-High levels of serum uric acid are associated with hypertension in observational studies. The aim of this study was to investigate the association of uric acid gene variants with blood pressure. We studied 5791 participants aged ≥55 years from the Rotterdam Study. Thirty gene variants identified for serum uric acid level were used to compile genetic risk score (GRS). We used linear regression models to investigate the association of the uric acid GRS with systolic and diastolic blood pressure in the whole study population and separately in participants with and without comorbidities and medication use. In the age-and sex-adjusted model, each SD increase in uric acid GRS was associated with 0.75 mm Hg lower systolic blood pressure (95% confidence interval, −1.31 to −0.19) and 0.42 mm Hg lower diastolic blood pressure (95% confidence interval, −0.72 to −0.13). The association did not attenuate after further adjustment for antihypertensive medication use and conventional cardiovascular risk factors. In subgroup analysis, the association of uric acid GRS with systolic blood pressure was significantly stronger in participants (n=885) on diuretic treatment (P for interaction, 0.007).In conclusion, we found that higher uric acid GRS is associated with lower systolic and diastolic blood pressure. Diuretics treatment may modify the association of uric acid genetic risk score and systolic blood pressure. Measurement of Serum Uric Acid and Blood PressureValues of serum uric acid were obtained from nonfasting blood samples, which were centrifuged for 10 minutes at 3000 rpm and subsequently stored at −20°C for 1 week. Uric acid activity was ascertained with Kone Diagnostica reagent kit and Kone autoanalyzer. To check the calibration, for every 10 samples, 3 control samples were included. In each run (100 samples), if the average values of the control samples were not within 2.5% of the true value, the run was repeated. Calibration was also done on day-by-day variation, which had to be within 5%. 10After a resting period of 5 minutes, blood pressure was measured twice in a single visit using a random-zero sphygmomanometer (cuff size of 32×17) on the right arm of participants in sitting position. The average of 2 measurements, separated by a count of the pulse rate, was used in the analyses. 11 CovariatesBody mass index was calculated by dividing weight in kilograms by height in meters squared. Information on alcohol consumption was acquired from the questionnaires. Participants were asked for the average daily consumption of alcohol. Medication use information was based on home interview. Diabetes mellitus was defined as the use of blood glucose-lowering medications or a random nonfasting glucose >11.1 mmol/L.12 Coronary heart disease was considered as having experienced myocardial infarction or undergone coronary revascularization procedures.13 Serum creatinine was determined using nonkinetic alkaline picrate (Jaffé) method. Estimated glomerular filtration rate was calculated using the simplified Modification of Di...

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“…Our result is similar to that of Bellomo et al, which reported that each increase of 10 mg/l (59 μmol/l) was associated with 23% risk of decreased GFR greater than 2 ml/min/year (after adjustment of confounding factors) in healthy normotensive adults [12]. A randomized clinical trial in hyperuricemic adolescents with hypertension (the decrease in uricemia under allopurinol was related to a decrease in blood pressure) changed the classic design where the cardiovascular drop-risk association in some studies was due to l Gout belongs to the metabolic syndrome [36].…”

Section: Discussionmentioning

confidence: 99%

Hyperuricemia in Patients with Chronic Renal Failure in the General Hospital of National Reference of N’Djamena (Chad)

Abderraman¹,

Hamat²,

Tondi³

et al. 2017

OJNeph

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Introduction: Hyperuricemia is defined as a level of serum uric acid greater than or equal to 70 mg/l (420 μmol/l) in men and 60 mg/l (360 μmol/l) in women. Several studies have shown that it is a risk factor or a factor of progression of chronic kidney disease. Recent experimental and epidemiological data correlate the association of hyperuricemia with chronic kidney disease (CKD), arterial hypertension and cardiovascular diseases, thus raising the question of the usefulness of therapeutics in the prevention of renal diseases. The objective of this study is to seek a link between chronic kidney disease and hyperuricemia. Materials and Methods: This is a descriptive and analytical study conducted at hemodialysis unit and cardiology service of General Hospital of National reference of N'Djamena (Chad) from 1 th January to 1 th October 2013 (10 months). We included all chronic kidney disease patients hospitalized in hemodialysis unit and cardiology service who presented associated hyperuricemia. Results: There were 712 CKD patients who were hospitalized. Among them, there were 108 patients who were included in the study and who had hyperuricemia as a prevalence of 15.20%. The average age of patients was 35.5 years and the sex ratio was 3/1. The age group between 40 to 60 years represented 54.6%. There were 41.7% of traders. Hypertensive patients accounted for 49.1%; association of diabetes and hypertension was noted in 12.90%. Renal insufficiency was moderate in 43.5% of patients. Hyperuricemia was present in more than 90% of patients. Profession, age, hematuria, proteinuria and hypertension were statistically positively related to 10hyperuricemia. Treatment consisted of prescribing allopurinol in 84% of patients. In more than 11% of patients the progression was unfavorable. Conclusion: The implication of hyperuricemia in chronic kidney disease has been proved in several recent studies. However, randomized studies at very long scales have to be carried out to conclude from its real impact on the prevention and treatment of chronic kidney disease.

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Uric Acid and Hypertension: Cause or Effect?

Cited by 126 publications

References 99 publications

The role of oxidative stress in the pathophysiology of hypertension

The role of oxidative stress in the pathophysiology of hypertension

Association of Uric Acid Genetic Risk Score With Blood Pressure

Hyperuricemia in Patients with Chronic Renal Failure in the General Hospital of National Reference of N’Djamena (Chad)

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