Hyperuricemia in Primary and Renal Hypertension

Cannon, Paul J.; Stason, William B.; Demartini, Felix E.; Sommers, Sheldon C.; Laragh, John H.

doi:10.1056/nejm196609012750902

Cited by 487 publications

(274 citation statements)

References 36 publications

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“…1 Although extensive epidemiological data suggest that serum uric acid (SUA) is a relevant marker for cardiovascular disease in different clinical settings including hypertension, it remains debatable whether SUA is an independent risk factor for adverse cardiovascular outcome. [2][3][4][5] Several pathophysiological mechanisms linking SUA to adverse cardiovascular outcome have been proposed, including proliferation of vascular smooth muscle cells, 6 prothrombotic effects mediated by platelet activation, 7 impaired nitric oxide generation and endothelial dysfunction, 8 activation of local renin-angiotensin-aldosterone system 9 and stimulation of inflammatory pathways.…”

Section: Introductionmentioning

confidence: 99%

The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives

et al. 2010

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The data regarding the role of serum uric acid (SUA) along with subclinical inflammation in the context of hypertensive vascular damage are rather scarce and controversial. Towards this end, we assess the links between SUA, high-sensitivity CRP (hs-CRP), adiponectin and carotid to femoral pulse wave velocity (c-f PWV) in 292 subjects with never-treated stage I-II essential hypertension. On the basis of the median SUA levels (0.31 mmol l À1 ), the study population was divided into subjects with low (n ¼ 149) and high (n ¼ 143) SUA values. By multiple regression analysis, it was revealed that SUA was independently associated with log hs-CRP (R 2 ¼ 0.098; P ¼ 0.02), log adiponectin (R 2 ¼ 0.102; P ¼ 0.03), waist circumference (R 2 ¼ 0.049; P ¼ 0.04), 24-h systolic blood pressure (SBP) (R 2 ¼ 0.179; P ¼ 0.001) and estimated glomerular filtration rate (R 2 ¼ 0.156; b (s.e.) ¼ À0.169 (0.023); P ¼ 0.02). In addition, c-f PWV was independently associated with age (R 2 ¼ 0.116; Po0.0001), waist circumference (R 2 ¼ 0.088; Po0.0001), 24-h SBP (R 2 ¼ 0.167; P ¼ 0.001), log adiponectin (R 2 ¼ 0.07; P ¼ 0.006) and log hs-CRP (R 2 ¼ 0.06; P ¼ 0.034). In conclusion, SUA levels are independently associated with hs-CRP and adiponectin levels but not with c-f PWV in essential hypertensive patients. Increased SUA levels are accompanied by a state of pronounced inflammatory activation and hypoadiponectinemia that significantly impairs the arterial stiffness accelerating the vascular ageing process in this setting.

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Section: Introductionmentioning

confidence: 99%

The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives

et al. 2010

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“…A quarter of untreated hypertensives, 50% of patients on diuretics and 475% of subjects with malignant HT or renal dysfunction have raised SUA. 12 SUA has been pathogenically linked to cardiovascular disease (CVD) and HT. Even when adjusted for traditional CV risk factors, age, race and use of diuretics, SUA is an independent, significant factor for the development of CVD in general, 13 and possibly in the RA population 6 and predicts approximately a twofold increase in the frequency of HT in the general population after 5-10 years.…”

Section: Introductionmentioning

confidence: 99%

Serum uric acid is independently associated with hypertension in patients with rheumatoid arthritis

et al. 2007

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“…6 In clinical studies, the association of high serum urate levels with the development of essential hypertension has been known for decades, but the underlying mechanisms are still unknown. 7,8 A significant association of plasma urate and xanthine oxidoreductase (XOR) activity with mean arterial blood pressure has been observed in clinical studies among normotensive individuals. 9 Urate is produced in purine catabolism from the ATP degradation products xanthine and hypoxanthine by XOR, which occurs as xanthine dehydrogenase (XDH, EC 1.1.1.204) and xanthine oxidase (XO, EC 1.2.3.2).…”

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confidence: 99%

Increased Kidney Xanthine Oxidoreductase Activity in Salt-Induced Experimental Hypertension

et al. 1998

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Abstract-Clinical and experimental studies have established an association between high sodium intake and arterial hypertension. The renal mechanisms resulting in impaired sodium excretion in hypertension-prone subjects are not clear. In hypertension-prone rats, high blood pressure results in increased renal mass and hemodynamic changes, both of which may alter renal oxygen distribution. Xanthine oxidoreductase (XOR) oxidizes ATP metabolites hypoxanthine and xanthine to urate. Because XOR is induced by hypoxia, we assessed kidney XOR activity in 2 models of salt-sensitive hypertension, spontaneously hypertensive rats (SHR) and Dahl salt-sensitive (Dahl S) rats. Increasing sodium intake from basal (0.08%) to high (2.56% wt/dry wt in the diet) increased renal XOR activity dose-dependently from 68Ϯ8 to 143Ϯ21 U/mg protein in the Dahl S (PϽ0.05) but not in Dahl salt-resistant (Dahl R) rats. On basal and high sodium diets, SHR had higher renal XOR activity (101Ϯ10 and 134Ϯ26 U/mg protein, respectively) than normotensive Wistar-Kyoto rats (55Ϯ2 and 58Ϯ6 U/mg protein, PϽ0.05). Sodium restriction (0.02% wt/wt) downregulated kidney XOR activity in both Dahl S and R rats by nearly 40%. In SHR, allopurinol treatment totally inhibited renal XOR activity, but neither systolic blood pressure nor renal mass changed. The results suggest that renal XOR induction is a consequence of increased salt intake or the resulting hypertension. However, further studies on renal XOR activity during the development of hypertension are needed to assess the importance of XOR in the pathophysiology of arterial hypertension. (Hypertension. 1998;32:902-906.)Key Words: hypertension, essential Ⅲ xanthine oxidoreductase Ⅲ rats, inbred SHR Ⅲ rats, Dahl Ⅲ hypertrophy Ⅲ sodium Ⅲ allopurinol I n salt-sensitive rats, increasing salt intake results in marked hypertension and left ventricular and renal enlargement within weeks. The genetically related salt-insensitive rats develop these harmful, sodium-induced effects to a much lesser extent.1-3 Kidney transplants derived from normotensive rats have been shown to decrease permanently the systolic blood pressure of an adult salt-sensitive recipient and also abolish the predisposition to hypertension in young animals.4,5 These observations, based on studies on the spontaneously hypertensive rat (SHR) and its normotensive control Wistar-Kyoto rat (WKY) as well as the Dahl saltsensitive (Dahl S) and salt-resistant (Dahl R) rat, indicate the crucial importance of the kidney in the pathogenesis of hypertension. Mechanisms resulting in an impaired excretion of sodium in relation to renal perfusion pressure in saltsensitive rat strains have not been fully worked out.

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Hyperuricemia in Primary and Renal Hypertension

Cited by 487 publications

References 36 publications

The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives

The diverse associations of uric acid with low-grade inflammation, adiponectin and arterial stiffness in never-treated hypertensives

Serum uric acid is independently associated with hypertension in patients with rheumatoid arthritis

Increased Kidney Xanthine Oxidoreductase Activity in Salt-Induced Experimental Hypertension

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