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The relaxation induced by oestrogen in the coronary vascular bed from normotensive rats has been well described. However, almost nothing is known about this action in spontaneously hypertensive rats (SHR). We investigated the effect of 17 β-oestradiol (E2) in coronary arteries from SHR as well as the contribution of the endothelium and the vascular smooth muscle to this action.Coronary arteries from male and female rats were used. Mean arterial pressure (MAP) and baseline coronary perfusion pressure (CPP) were determined. The effects of 10 μm E2 were assessed by in bolus administration before and after endothelium denudation (0.25 μm sodium deoxycholate) or perfusion with 100 μm Nω-nitro-l-arginine methyl ester (l-NAME), 2.8 μm indomethacin, 0.75 μm clotrimazole, 100 μm l-NAME after endothelium denudation (0.25 μm sodium deoxycholate), 100 μm l-NAME plus 2.8 μm indomethacin, 0.75 μm clotrimazole plus 2.8 μm indomethacin and 4 mm tetraethylammonium (TEA).MAP was higher in the male group, while CPP was higher in the female group (P < 0.05). There were no differences in E2-induced relaxation between females and males (−17 ± 1.6 vs. −17 ± 2% respectively). Only in the female group the E2 response was significantly attenuated after endothelium removal or perfusion with clotrimazole. The response to E2 was reduced in both groups with l-NAME, l-NAME plus indomethacin, l-NAME after endothelium removal or TEA.Nitric oxide, endothelium-derived hyperpolarizing factor and potassium channels may have the most important role to E2 response in the female group, whereas nitric oxide and potassium channels may have the most important role in the male group.