Vol 9, No 4 (2005)
Original paper
Published online: 2005-08-05

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PAI-1 and hyperuricaemia: another face of endothelium dysfunction in essential hypertension. Endothelium, hypertension, metabolism

Marek Kretowicz, Małgorzata Ukleja-Adamowicz, Paweł Stróżecki, Krzysztof Buczkowski, Katarzyna Klucz, Ryszard Paczuski, Grażyna Odrowąż-Sypniewska, Jacek Manitius
Nadciśnienie tętnicze 2005;9(4):261-265.


Background Attention is increasingly being paid to endothelial dysfunction (ED) as a key aspect of atherosclerosis and target organ damage in arterial hypertension.
Material and methods In order to evaluate generalised ED in non-diabetic untreated essential hypertensives with normal creatinine clearance we examined 29 ambulatory patients (13F/16M; age: 41.17 ± 11.95) and compared them with 14 healthy controls (7F/7M) matched for age. Fasting blood was withdrawn for the following: HbA1c, total homocysteine, uric acid, insulin, glucose, vWF:Ag, TM, PAI-1 and E-selectins in both groups. HOMA-IR was calculated. 24-h urine was collected for microalbuminuria (MA) and N-acetyl-ß-D-glucosaminidase (NAG) urine excretion.
Results The hypertensives had higher BMI, WHR, MAP and PP and were insulin resistant. They revealed hyperuricaemia. No difference was found in MA and vWF:Ag.
The hypertensives also had higher PAI-1 levels and NAG excretion than the controls. The only positive linear correlations found in the hypertensives were the following: PP vs. MAlog10, PAI-1 vs. MAlog10, PAI-1 vs. uric acid, PAI-1 vs. BMI, PAI-1 vs. WHR, WHR vs. uric acid, BMI vs. HOMA-IR.
Conclusion Our data may suggest that in the early stages of essential hypertension patients with insulin resistance are at high risk of serious cardiovascular complications related to diffuse atherosclerosis, a prothrombotic state and elevated arterial stiffness. Uric acid is able to affect endothelium through a PAI-1 mediated mechanism, which remains unclear. This fact is reflected in the increased PP which results from increased arterial stiffness. Higher NAG urine excretion where there is no endothelial dysfunction may indicate the early renal tubulo-interstitium tissue damage which precedes glomerular injury and is important for future clinical prognosis.

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