Fig. 2.
Fig. 2. Real-time representation of 10−9 mol/L 17β-estradiol–stimulated [Ca2+]i and NO release from human granulocytes. / (A) Real time representation of 10−9 mol/L 17β-estradiol–stimulated NO release from peripheral granulocytes and its blockade by 10−9 mol/L tamoxifen (Tam) but not 10−8 mol/L ICI-182,780 (ICI). Tamoxifen and ICI-182,780 were administered 2 minutes prior to 17β-estradiol. (B) 17β-Estradiol–stimulated [Ca2+]i (Est) and its antagonist. Tamoxifen (Tam; 10−9 mol/L) antagonizes 17β-estradiol–stimulated [Ca2+]i, but 10−8 mol/L ICI-182,780 (ICI) does not. Drugs were administered as in (A). (C) 17β-Estradiol–stimulated [Ca2+]i (Est) and its BAPTA-AM concentration-dependent decrease, which demonstrates that [Ca2+]i transients are associated with estradiol's action. (D) Confocal laser photomicrograph of E2-BSA-FITC reactivity of the cell surface of granulocytes (right) and control granulocyte (left).

Real-time representation of 10−9 mol/L 17β-estradiol–stimulated [Ca2+]i and NO release from human granulocytes.

(A) Real time representation of 10−9 mol/L 17β-estradiol–stimulated NO release from peripheral granulocytes and its blockade by 10−9 mol/L tamoxifen (Tam) but not 10−8 mol/L ICI-182,780 (ICI). Tamoxifen and ICI-182,780 were administered 2 minutes prior to 17β-estradiol. (B) 17β-Estradiol–stimulated [Ca2+]i (Est) and its antagonist. Tamoxifen (Tam; 10−9 mol/L) antagonizes 17β-estradiol–stimulated [Ca2+]i, but 10−8 mol/L ICI-182,780 (ICI) does not. Drugs were administered as in (A). (C) 17β-Estradiol–stimulated [Ca2+]i (Est) and its BAPTA-AM concentration-dependent decrease, which demonstrates that [Ca2+]i transients are associated with estradiol's action. (D) Confocal laser photomicrograph of E2-BSA-FITC reactivity of the cell surface of granulocytes (right) and control granulocyte (left).

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