Affiliation:
1. From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing.
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 H
2
O
2
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 H
2
O
2
was 3 times greater in DOCA aorta compared with sham aorta but unchanged in DOCA vena cava compared with sham vena cava. In prostaglandin F
2α
(20 μmol/L)–contracted aorta and vena cava from sham and DOCA rats, H
2
O
2
(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 H
2
O
2
-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 H
2
O
2
-induced contraction, whereas only ouabain enhanced venous H
2
O
2
-induced contraction. The removal of extracellular Ca
2+
reduced H
2
O
2
-induced contraction in KCl-contracted aorta, whereas maximal venous H
2
O
2
-induced contraction (under basal conditions) was unchanged. Our data suggest that differences in arterial and venous K
+
channel activity and extracellular Ca
2+
influx are responsible for differences in arterial and venous contraction to H
2
O
2
. In DOCA-salt hypertension, arterial but not venous contraction to H
2
O
2
is enhanced, and relaxation to H
2
O
2
is reduced.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Cited by
38 articles.
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