vascular endothelium, the molecular mechanism responsible for this effect remains to be
elucidated. In studies of both human umbilical vein endothelial cells (HUVECs) and simian
virus 40-transformed rat lung vascular endothelial cells (TRLECs), 17β-estradiol (E2), but
not 17α-E2, caused acute activation of eNOS that was unaffected by actinomycin D and was
specifically blocked by the pure estrogen receptor antagonist ICI-182,780. Treatment of both …