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Cardiovascular disease (CVD) is a major source of morbidity and mortality in the Western World. Premenopausal and estrogen-treated postmenopausal women have a lower incidence of CVD. It has been suggested that circulating endogenous estrogens are probably responsible for this protection. This study investigated the hypothesis that the reduction of endothelial permeability is responsible for cardioprotective effects of estrogen in hypertensive animals. Fourty-four rats were ovariectomized and divided into five groups: groups 1, 2 and 4 received DOCA-salt and groups 3 and 5 received normal saline (N/S) injection for four weeks. Then, in groups 4 and 5 the blood pressure was measured. Group 1 received estradiol valerate and in groups 2 and 3 continued with DOCA-salt and N/S injection for six weeks, respectively. Endothelial permeability was measured by Evans Blue extraction method. There was no significant difference in endothelial permeability in coronary circulation in estrogen-treated group and controls (12.97+/-2.32 vs. 9.96+/-1.01, respectively). Also, aortic endothelial permeability in DOCA-salt hypertensive rats did not change significantly after estrogen treatment (28.34+/-3.65 vs. 41.60+/-5.98). This study showed that the cardioprotective effects of estrogen in DOCA-salt hypertensive animals are not mediated by a reduction of endothelial permeability.