THE EFFECT OF ESTROGEN AND PROGESTERONE ON BETA-ADRENERGIC-RECEPTOR ACTIVITY IN RABBIT LUNG-TISSUE

Study of the effect of sex steroids on the development of .beta.-adrenergic receptors may be essential to an understanding of the mechanisms of both lung maturation and the initiation of labor. (3H)Dihydroalprenolol (DHA) was used to quantify .beta.-adrenergic receptor sites in mature and immature rabbit lung tissue. DHA binding was rapid, saturable, of high affinity (Kd = 2 nM), and of low capacity (246-576 f[femto]mol/mg of protein), and adrenergic competitors demonstrated both stereoselectivity ([-]isomer .mchgt. [+]isomer) and a rank order of potency (isoproterenol .mchgt. norepinephrine > epinephrine) characteristic of the .beta.-adrenergic receptor. .beta.-Adrenergic receptors in the lung tissue of both mature and immature female New Zealand White rabbits were investigated under various sex steroid situations. Estrogen (diethylstilbestrol, 5 .mu.g/day for 10 days) increased the .beta.-adrenergic receptor site number in immature rabbits compared to matched controls (435 vs. 339 fmol/mg of protein, P < 0.02 by paired t-test). Addition of progesterone (diethylstilbestrol, 5 .mu.g for 10 days, plus progesterone, 5 mg/day for 3 days) returned the .beta.-adrenergic receptor site number to control values (321 fmol/mg of protein, P < 0.01). In mature rabbits, treatment with progesterone alone (10 mg/day for 4 days) caused a significant reduction in 7b-adrenergic receptor site numbers compared to untreated, matched controls (357 vs. 493 fmol/mg of protein, P < 0.05 by paired t-test). In the presence of estrogen, .beta.-adrenergic receptor activity is enhanced in both mature and immature rabbit lung tissue. Addition of progesterone restores this activity to control values.