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Am J Physiol Heart Circ Physiol (May 23, 2008). doi:10.1152/ajpheart.00304.2008
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Submitted on March 20, 2008
Revised on April 23, 2008
Accepted on May 12, 2008

Xanthine Oxidase and Mitochondria Contribute to Vascular Superoxide Anion Generation in DOCA-Salt Hypertensive Rats

Emilie C Viel1, Karim Benkirane1, Danesh Javeshghani, Rhian M. Touyz2, and Ernesto L Schiffrin3*

1 Lady Davis Institute for Medical Research, Sir Mortimer B. Davis-Jewish General Hospital
2 University of Ottawa
3 Lady Davis Institute, McGill University

* To whom correspondence should be addressed. E-mail: ernesto.schiffrin{at}mcgill.ca.

Vascular superoxide anion (•O2-) levels are increased in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. We hypothesized that endothelin-1 (ET-1)-induced generation of reactive oxygen species (ROS) in aorta and resistance arteries of DOCA-salt rats originates partly from xanthine oxidase and mitochondria. Accordingly, we blocked xanthine oxidase and the mitochondrial oxidative phosphorylation chain to investigate their contribution to ROS production in mesenteric resistance arteries and aorta from DOCA-salt rats. Systolic blood pressure rose in DOCA-salt rats and was reduced after 3 weeks by apocynin (NAD(P)H inhibitor and/or radical scavenger), allopurinol (xanthine oxidase inhibitor), bosentan (ETA/B receptor antagonist), BMS182874 (ETA receptor antagonist) and hydralazine. Plasma uric acid levels in DOCA-salt rats were similar to control unilaterally nephrectomised (UniNx) rats, reduced with allopurinol and bosentan and increased with BMS. Levels of thiobarbituric acid reacting substances (TBARS) were increased in DOCA-salt rats versus UniNx rats, and BMS, bosentan and hydralazine prevented their increase. Dihydroethidium staining showed reduced •O2- production in mesenteric arteries and aorta from BMS and bosentan-treated compared to untreated DOCA-salt rats. Increased •O2- derived from xanthine oxidase was reduced or prevented by all treatments in mesenteric arteries, whereas bosentan and BMS had no effect on aorta from DOCA-salt rats. •O2- generation decreased with in situ treatment by tenoyltrifluoroacetone and carbonyl cyanide-m-chlorophenylhydrazone, inhibitors of mitochondrial electron transport complexes II and IV respectively, whereas rotenone (mitochondrial complex I inhibitor) had no effect. Our findings demonstrate involvement of ETA receptor-modulated •O2- derived from xanthine oxidase and from mitochondrial oxidative enzymes in arteries from DOCA-salt rats.




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[Abstract] [Full Text] [PDF]


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