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The effects of pregnancy or progesterone dominance on the β-adrenergic responsiveness of the uterus were studied in myometrial membranes from mid-and late-pregnant rats (day 15 and on the 16th h of day 22 of pregnancy respectively) or 24 h after administration of progesterone. Levels of the high (R_H)- and low (R_L)-affinity states of the β-adrenergic receptor were determined by competition experiments between ¹²⁵I-labelled cyanopindolol binding and the selective β-agonist isoproterenol. The ratio K_L/K_H (respective dissociation constants) was determined since it also reflects the degree of formation of the high-affinity state of the β-adrenergic receptor. From day 15 to the 10th h of day 22 of pregnancy, two distinct affinity states were apparent: 80–55% R_H (K_H=0·31–0·21 µM) and 45–20% R_L (K_L=14–5 µM) with a ratio of K_L/K_H of 55–34. In the last 6 h before birth, β-adrenergic receptors underwent uncoupling which was paralleled by decreased responsiveness of myometrial adenylate cyclase to isoproterenol (maximum velocity (V_max)=17±3 vs 44±3 fmol cyclic AMP/10 min per mg protein on day 15). At this stage of pregnancy, previous exposure to progesterone resulted in a 1·8-fold increase in ¹²⁵I-labelled cyanopindolol-binding sites (B_max) and the reappearance of the high-affinity state (67% R_H, K_H=0·19±0·04 (S.E.M.) µM, ratio K_L/K_H=81·1 ± 16·9). These results were reversed in the presence of the antiprogestin RU486 (100% R_L, K_L=24·6±4·1 µM, 41% reduction of B_max). Moreover, after progesterone, adenylate cyclase activity was strongly stimulated by isoproterenol (V_max=60±12 fmol cyclic AMP/10 min per mg protein vs 17±3 in controls). The data suggest (1) that progesterone may exert a permissive effect on β-adrenergic responsiveness of the pregnant rat myometrium and (2) that at term, both a desensitization mechanism involving uncoupling of β-adrenergic receptors and a decrease in activation of adenylate cyclase lead to a loss of myometrial response to β-agonists.

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