Role of Xanthine Oxidase in Dexamethasone-Induced Hypertension in Rats

Abstract

1. Glucocorticoid-induced hypertension (GC-HT) in the rat is associated with nitric oxide-redox imbalance. 2. We studied the role of xanthine oxidase (XO), which is implicated in the production of reactive oxygen species, in dexamethasone-induced hypertension (dex-HT). 3. Thirty male Sprague-Dawley rats were divided randomly into four treatment groups: saline, dexamethasone (dex), allopurinol plus saline, and allopurinol plus dex. 4. Systolic blood pressures (SBP) and bodyweights were recorded each alternate day. Thymus weight was used as a marker of glucocorticoid activity, and serum urate to assess XO inhibition. 5. Dex increased SBP (110 ± 2-126 ± 3 mmHg; P < 0.001) and decreased thymus (P < 0.001) and bodyweights (P′ < 0.01). Allopurinol decreased serum urate from 76 ± 5 to 30 ± 3 μmol/L (P < 0.001) in saline and from 84 ± 13 to 28 ± 2 μmol/L in dex-treated (P < 0.01) groups. 6. Allopurinol did not prevent dex-HT. This, together with our previous findings that allopurinol failed to prevent adrenocorticotrophic hormone induced hypertension, suggests that XO activity is not a major determinant of GC-HT in the rat.