Alpha adrenergic responses of blood vessels of rabbits after ovariectomy and administration of 17β-estradiol

Experiments were designed to determine the effect of estrogen pretreatment on alpha adrenergic responsiveness of blood vessels of the rabbit. Rabbits were ovariectomized and, after 8 days of recovery, treated with 17β-estradiol (100 μg i.m.; estrogen group) or solvent (control group) for 4 days. Rings of saphenous vein and femoral artery (both without endothelium) were mounted for isometric tension recording in organ chambers filled with modified Krebs-Ringer bicarbonate solution (37°C), gassed with 95% O₂-5% CO₂. All experiments were performed in the presence of inhibitors of neuronal uptake, extraneuronal uptake and beta adrenoceptors. In the saphenous vein, the estrogen treatment did not significantly affect the concentration-effect curves evoked by norepinephrine (either under control conditions or after alpha-1 or alpha-2 adrenergic blockade), phenylephrine (an alpha-1 adrenergic agonist) or UK 14,304 (an alpha-2 adrenergic agonist). In the femoral artery, estrogen treatment depressed the contractile responses evoked by norepinephrine (under control conditions) but not those produced by phenylephrine; UK 14,304 did not evoke a contractile response. The depressant effect of estrogen treatment on the concentration-effect curve to norepinephrine in the femoral artery was prevented by the alpha-2 adrenergic antagonist, rauwolscine. The results in the femoral artery but not in the saphenous vein suggest that estrogens depress alpha-2 but not alpha-1 adrenergic responsiveness. In the femoral artery, alpha-2 adrenoceptor stimulation does not cause contraction per se but apparently can facilitate alpha-1 adrenergic responses. This probably results from a reduced density of alpha-2 adrenoceptors in this blood vessel. Thus, the inhibitory influence of estrogen on alpha adrenergic responses of vascular smooth muscle may depend on the density of adrenoceptors (or spare receptors).