17β-estradiol increases intracellular calcium concentration through a short-term and nongenomic mechanism in rat vascular endothelium in culture

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 E₂ at 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 E₂ on [Ca²⁺](i) kinetics. 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 C(β) activity is involved in these effects, because U-73122, a PLC(β) inhibitor, blocked E₂ effects. All E₂ effects 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.