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17β-Estradiol (E2) plays an important role in Ca2+fluxes in several cell types. It has been proposed that some of its effects are of nongenomic origin E2at vascular smooth muscle level can block calcium entry through L-type calcium channels, this mechanism cannot include vascular endothelial cells (VECs), in which increases in the intracellular calcium concentration (Ca2+i) are necessary to NO synthesis. We used male rat aorta ECs in culture loaded with fura-2 and a fluorescence imaging system to evaluate the short-term effects of E2on Ca2+ikinetics. We explored the participation of the intracellular steroid receptor on the effects induced by E2, using tamoxifen (1 μM) and ICI 182,780 (10 μM). Our results showed that E2(like bradykinin) induced an increase in Ca2+i. Such agonist-like effects showed a biphasic curve behavior. The 17β-estradiol effects were not modified by the presence of the intracellular estradiol-receptor antagonist tamoxifen, but it is blocked in the presence of the ICI 182,780. The 17β-estradiol effects were obtained even with restriction of steroid-free diffusion into cells (17β-estradiol-bovine serum albumin). Phospholipase Cβactivity is involved in these effects, because U-73122, a PLCβinhibitor, blocked E2effects. All E2effects were of rapid onset (milliseconds), exerted at the membrane level, and of rapid offset. We conclude that estradiol can influence the endothelium physiologic responses through effects of nongenomic origin.