Physiologic significance of 17beta-estradiol binding in the rabbit Fallopian tube.

Rabbit Fallopian tube contractility was recorded in vitro during perfusion with either Locke's solution or that solution containing CN-55, 945-27 (CN; or CI-628), a nonsteroidal estrogen antagonist (Endocrinology 79: 153, 1966). Contractility was inhibited and 17beta-estradiol (E2) displaced from both its cytoplasmic (8S) and nuclear (4S) receptors in the presence of the above agent. These effects result from a direct interaction between CN and the E2-receptor complexes. Two types of evidence show the specificity of the foregoing responses: (1) nonspecific binding of E2 to serum proteins was unaffected by the antagonist and (2) CN had no effect on contractility of a nontarget tissue, i.e., rabbit ileum. In addition, Fallopian tube contractions induced by strong electrical stimulation of K-depolarized tissues (i.e., in the absence of normal ionic gradients) were inhibited by CN and a decrease in the binding capacities of 8S and 4S receptors was again observed. Thus, antagonism of specific E2 binding inhibits the contractile mechanism at a level other than the cell membrane. These observations, and additional findings concerning the reversibility of CN action, indicate that E2 binding is essential for contractility of the rabbit Fallopian tube.