The Effect of Ovarian Hormones on the Contractility of the Rabbit Oviductal Isthmus

Abstract

In order to investigate the phenomenon of "tubal locking" of ova, the in vitro contractility of circular rings from the rabbit oviductal isthmus was examined in different hormonal states. Both alpha and beta adrenergic receptors were found to be present in this preparation with predominance of the alpha receptors when the tissues were from either estrogen- or progesterone-dominant animals.Progesterone treatment of estrogen-primed, immature females influenced the dose–response curve of the circular oviductal muscle to norepinephrine, significantly shifting it to the right, in comparison with tissues from animals that had been treated with estrogen only. There was less of a shift when dose–response relations were determined for phenylephrine after beta receptor blocked with propranolol, suggesting that progesterone enhanced the responses of beta compared with alpha receptors. However, there was still a small difference between responses of estrogen- and progesterone-dominated tissue, at least at low concentrations. Since beta receptor activity had been effectively eliminated, this tendency suggests that progesterone's effect on the response to norepinephrine is not completely due to a modification in beta receptor activity.The spontaneous contractility of tissues from estrogen-treated animals was characterized by a series of rapid spike-like contractions with fairly consistent shape and frequency. Additional treatment with progesterone modified the pattern to an irregular one. Moreover, the total spontaneous activity of muscle from estrogen-dominant animals (as measured by the area under the contractility curve) was significantly reduced, and the rate of tension increase was considerably slower than that from animals with progesterone as the dominant hormone. This indicated a form of antagonism to estrogen by progesterone not involving adrenergic receptors.Maximal excitation of the strips with nonspecific agents or adrenergic agonists resulted in significantly less activity in tissues from progesterone-treated animals. The mechanism of action of progesterone to produce this effect probably involves a step or steps in the excitation–contraction process beyond the adrenergic receptors.