Endothelium-derived factors play an important role in vascular tone control. This study aimed to evaluate how endothelium and reactive oxygen species (ROS) contribute to phenylephrine (PE)-induced contraction in renovascular hypertensive (2K-1C) and normotensive (2K) rats aortas. The effects of the superoxide scavenger Tiron (0.1mM and 1mM) or catalase (30 U/ml, 90 U/ml, 150 U/ml and 300 U/ml) on the PE-induced contraction were evaluated in both intact endothelium (E+) and denuded (E-) aortas. Endothelium removal increased the PE-induced contractions. The maximum contractile response decreased only in 2K-1C rat E+ aorta, and catalase (30 U/ml, 90 U/ml, 150 U/ml) partially reversed this effect. Endothelium increased the basal hydrogen peroxide (H2O2) production in 2K and 2K-1C rats aortas. PE-stimulated H2O2 production was higher in 2K-1C (E+/E-) than in 2K (E+/E-). Inhibition of the enzymes cyclooxygenase, NADPH-oxidase, xanthine-oxidase, and superoxide dismutase reduced the PE-stimulated H2O2 production in 2K-1C rat aorta. The decreased contraction to PE in 2K-1C rat aorta is partially due to endothelial H2O2 production; however, in denuded aorta, it contributes to maintaining the contractile response. Superoxide plays an important role on the PE-induced contraction in 2K rat denuded aorta, whereas in 2K-1C rat aorta, it is H2O2 that plays an important role in this effect.
Keywords: 2K–1C renal hypertension; Adrenergic α(1) agonist; Contractile response; Endothelial factor; Oxygen radical.
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