Role of xanthine oxidase in dexamethasone-induced hypertension in rats

Sharon L.H. Ong; Janine J. Vickers; Yi Zhang; Katja U.S. McKenzie; Claire E. Walsh; Judith A. Whitworth

doi:10.1111/j.1440-1681.2007.04605.x

Role of xanthine oxidase in dexamethasone-induced hypertension in rats

Sharon L.H. Ong, Janine J. Vickers, Yi Zhang, Katja U.S. McKenzie, Claire E. Walsh, Judith A. Whitworth^*

^*Corresponding author for this work

Research output: Contribution to journal › Article › peer-review

31 Citations (Scopus)

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.

Original language	English
Pages (from-to)	517-519
Number of pages	3
Journal	Clinical and Experimental Pharmacology and Physiology
Volume	34
Issue number	5-6
DOIs	https://doi.org/10.1111/j.1440-1681.2007.04605.x
Publication status	Published - May 2007

Access to Document

10.1111/j.1440-1681.2007.04605.x

Cite this

@article{cf4e0574013a46daa5dd57609b3c9707,

title = "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.",

keywords = "Allopurinol, Dexamethasone, Glucocorticoid, Hypertension, Reactive oxygen species, Superoxide, Xanthine oxidase",

author = "Ong, {Sharon L.H.} and Vickers, {Janine J.} and Yi Zhang and McKenzie, {Katja U.S.} and Walsh, {Claire E.} and Whitworth, {Judith A.}",

year = "2007",

month = may,

doi = "10.1111/j.1440-1681.2007.04605.x",

language = "English",

volume = "34",

pages = "517--519",

journal = "Clinical and Experimental Pharmacology and Physiology",

issn = "0305-1870",

publisher = "Wiley-Blackwell Publishing Ltd",

number = "5-6",

}

TY - JOUR

T1 - Role of xanthine oxidase in dexamethasone-induced hypertension in rats

AU - Ong, Sharon L.H.

AU - Vickers, Janine J.

AU - Zhang, Yi

AU - McKenzie, Katja U.S.

AU - Walsh, Claire E.

AU - Whitworth, Judith A.

PY - 2007/5

Y1 - 2007/5

N2 - 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.

AB - 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.

KW - Allopurinol

KW - Dexamethasone

KW - Glucocorticoid

KW - Hypertension

KW - Reactive oxygen species

KW - Superoxide

KW - Xanthine oxidase

UR - http://www.scopus.com/inward/record.url?scp=33947660100&partnerID=8YFLogxK

U2 - 10.1111/j.1440-1681.2007.04605.x

DO - 10.1111/j.1440-1681.2007.04605.x

M3 - Article

SN - 0305-1870

VL - 34

SP - 517

EP - 519

JO - Clinical and Experimental Pharmacology and Physiology

JF - Clinical and Experimental Pharmacology and Physiology

IS - 5-6

ER -

Role of xanthine oxidase in dexamethasone-induced hypertension in rats

Abstract

Access to Document

Other files and links

Fingerprint

Cite this