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on January 23, 2006

A more recent version of this article appeared on March 1, 2006

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Submitted on November 28, 2005
Revised on December 12, 2005

Pleiotropic Effects of Hydrogen Peroxide in Arteries and Veins From Normotensive and Hypertensive Rats

Keshari Thakali^*; Lauren Davenport; Gregory D. Fink; and Stephanie W. Watts

From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing.

^* To whom correspondence should be addressed. E-mail: thakalik{at}msu.edu.

Abstract--Hydrogen peroxide causes vascular contraction and relaxation and contributes to the pathogenesis of hypertension. We hypothesized that the contractile state of blood vessels governs whether H₂O₂ causes contraction or relaxation. Hydrogen peroxide (1 µmol/L to 1 mmol/L) concentration-dependently contracted thoracic aorta and vena cava from sham normotensive and deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The maximal contraction to H₂O₂ was 3 times greater in DOCA aorta compared with sham aorta but unchanged in DOCA vena cava compared with sham vena cava. In prostaglandin F₂ (20 µmol/L)-contracted aorta and vena cava from sham and DOCA rats, H₂O₂ (1 µmol/L to 1 mmol/L) induced a concentration-dependent relaxation that was impaired in DOCA aorta but not DOCA vena cava. In contrast, in KCl (30 mmol/L)-contracted vessels, maximal H₂O₂-induced contraction was enhanced 15-fold in sham aorta and 5-fold in DOCA aorta but only 2-fold in sham vena cava. Tetraethylammonium (10 mmol/L), BAY K 8644 (100 nmol/L), and ouabain (1 mmol/L) all enhanced maximal aortic H₂O₂-induced contraction, whereas only ouabain enhanced venous H₂O₂-induced contraction. The removal of extracellular Ca²⁺ reduced H₂O₂-induced contraction in KCl-contracted aorta, whereas maximal venous H₂O₂-induced contraction (under basal conditions) was unchanged. Our data suggest that differences in arterial and venous K⁺ channel activity and extracellular Ca²⁺ influx are responsible for differences in arterial and venous contraction to H₂O₂. In DOCA-salt hypertension, arterial but not venous contraction to H₂O₂ is enhanced, and relaxation to H₂O₂ is reduced.

Key words: contraction • relaxation • arteries • veins

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