Figure 3
Original recordings demonstrating typical effect of 17α-E2 on uterine contractions. The inhibitory effect of 17α-E2 on spontaneous contractility was not blocked by preincubation with inhibitors of transcription, 10 μM actinomycin D (A) and protein synthesis, 100 μM cycloheximide (B) or antiestrogens, 1 μM tamoxifen or 1 μM ICI 182,780 (C and D, respectively). The vehicle utilized to add each compound, absolute ethanol (ETOH 0.1%), did not affect (P > 0.05) the spontaneous contractility (E). KCl-induced contraction was inhibited by addition of 5 μM noradrenaline (NA), which was antagonized by preincubation with β2-adrenoceptor antagonist, 20 μM propranolol (P), while 17α-E2-induced relaxation was not antagonized by P (F). The relaxing efficacy of estrogen was not modified in tissues pretreated with these blocking agents. The calcium-induced contraction at 1 mM (Ca2+) in tissues previously depolarized by high potassium-calcium free solution (KCl-Ca2+φ) was notably prevented by 17α-E2 (G). The solid black line indicates the incubation time with 17α-E2 at 89.39 μM. Note the contraction recovery after washout (represented by the black circles), showing that the estrogen effect was reversible.