1 The present study analyses the in¯uence of hypertension and endothelium on the e ect induced by hydrogen peroxide (H 2 O 2 ) on basal tone in aortic segments from normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR) of 6-month-old, as well as the possible mechanisms involved. 2 Single (1 mM) or cumulative (100 nM ± 10 mM) concentrations of H 2 O 2 produced a transient contraction or a concentration-dependent increase of basal tone, respectively, in segments from WKY and SHR. In both cases, the contractions were higher in intact segments from hypertensive than from normotensive rats, and increased by endothelium removal in both strains. Catalase (1000 u ml 71 , a H 2 O 2 scavenger) abolished the contraction elicited by 1 mM H 2 O 2 in both strains. 3 Superoxide dismutase (SOD, 150 u ml 71 ) and dimethylsulphoxide (DMSO, 7 mM), scavengers of superoxide anions and hydroxyl radicals, respectively, did not alter H 2 O 2 -induced contractions in intact segments from both strains. However, L-N G -nitroarginine methyl ester (L-NAME, 100 mM, a nitric oxide synthase inhibitor) increased the response to H 2 O 2 in normotensive rats, although the increase was less than that produced by endothelium removal. 4 Incubation of segments with 1 mM H 2 O 2 for 15 min and subsequent washout reduced the contractile responses induced by 75 mM KCl in intact segments from SHR and in endothelium-denuded segments from both strains; this e ect being prevented by catalase (1000 u ml 71 ). 5 Indomethacin (10 mM, a cyclo-oxygenase inhibitor) and SQ 29,548 (10 mM, a prostaglandin H 2 / thromboxane A 2 receptor antagonist) practically abolished the contractions elicited by H 2 O 2 in normotensive and hypertensive rats. 6 We conclude that: (1) the oxidant stress induced by H 2 O 2 produces contractions mediated by generation of a product of the cyclo-oxygenase pathway, prostaglandin H 2 or more probably thromboxane A 2 , in normotensive and hypertensive rats; (2) oxygen-derived free radicals are not involved in the e ect of H 2 O 2 ; (3) in normotensive rats, endothelium protects against H 2 O 2 -mediated injury to contractile machinery, determined by the impairment of KCl-induced contractions; and (4) endothelial nitric oxide has a protective role on the contractile e ect induced by H 2 O 2 , that is lost in hypertension.

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