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Related Experiment Videos

Uric acid and endothelial dysfunction in essential hypertension.

Carmine Zoccali1, Raffaele Maio, Francesca Mallamaci

  • 1CNR-IBIM Consiglio Nazionale delle Ricerche, Istituto di Biomedicina, delle Malattie Renali e dell'Ipertensione Arteriosa, c/o Divisione di Nefrologia e Dialisi, Ospedali Riuniti Via Vallone Petrara, Reggio Calabria, Italy.

Journal of the American Society of Nephrology : JASN
|April 14, 2006
PubMed
Summary

High uric acid (UA) levels are linked to poor endothelial function in hypertensive patients. This suggests UA may contribute to vascular damage, independent of other risk factors.

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Area of Science:

  • Cardiovascular Medicine
  • Nephrology
  • Vascular Biology

Background:

  • Serum uric acid (UA) is increasingly recognized as a risk factor for cardiovascular and renal diseases.
  • Endothelial dysfunction is an early indicator of cardiovascular events, especially in hypertension.

Purpose of the Study:

  • To investigate the association between serum UA and endothelial function in never-treated hypertensive patients.
  • To determine if UA is an independent predictor of endothelial dysfunction.

Main Methods:

  • Studied 217 white never-treated hypertensive patients (108 men, 109 women; age 48.0 ± 10.6 yr).
  • Assessed blood pressure, serum creatinine, C-reactive protein (CRP), insulin resistance (homeostasis model assessment), and serum UA.
  • Evaluated endothelial function via intra-arterial acetylcholine (ACh) infusion to measure vasodilatory response.

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Main Results:

  • Serum UA, serum creatinine, and CRP were significantly correlated with endothelial function (P < 0.0001).
  • In multiple regression analysis, serum UA was the third strongest predictor of forearm blood flow, after homeostasis model assessment and CRP.
  • An independent association between serum UA and endothelial function was observed, even after adjusting for CRP.

Conclusions:

  • Serum UA shows an inverse and significant relationship with ACh-stimulated vasodilation in untreated essential hypertension.
  • This link between UA and endothelial dysfunction appears independent of traditional cardiovascular risk factors.
  • Chronic inflammation may be the underlying mechanism connecting serum UA to vascular damage.