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ROLE OF XANTHINE OXIDASE IN DEXAMETHASONE‐INDUCED HYPERTENSION IN RATS
Author(s) -
Ong Sharon LH,
Vickers Janine J,
Zhang Yi,
McKenzie Katja US,
Walsh Claire E,
Whitworth Judith A
Publication year - 2007
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.2007.04605.x
Subject(s) - allopurinol , xanthine oxidase , endocrinology , medicine , dexamethasone , glucocorticoid , saline , chemistry , nitric oxide , xanthine , blood pressure , enzyme , biochemistry
SUMMARY1 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.