Effects in vitro of progesterone and estradiol-17.BETA. on the contractile and electrical responses in rat myometrium.

Abstract

Uterine longitudinal and circular muscles from pre-and postterm rats were studied in vitro for their contractile and electrical activities under the influence of 20-100 ,uM progesterone, 20 ,uM estradioll7R, or 20 ,uM stilbestrol. Uterine longitudinal or circular muscle strips were irrigated by Krebs solution at 37°C containing one of the hormones mentioned above, dissolved by the use of ultrasonic wave. Muscle contractions were recorded by a force displacement transducer, and electrical activities of the muscle membrane were studied using an intracellular microelectrode. At diestrus and Day 14 of pregnancy, progesterone depressed the contractions of longitudinal muscle. At pre-term, progesterone potentiated the contractions and prolongated the membrane burst discharge of longitudinal muscles, while estradiol inhibited their contractions and suppressed spike activities. At the same stage of pregnancy, both progesterone and estradiol inhibited contractions of circular muscles. At post-partum, progesterone potentiated and then depressed longitudinal muscles, while estradiol inhibited their contractions. At this stage, both progesterone and estradiol inhibited contractions of circular muscles, although vigorous spike discharges were observed. Stilbestrol depressed contractions of both longitudinal muscles from diestrus rats and longitudinal ileal muscles from a guinea pig. In view of these findings, it was deduced that these ovarian hormones exert dual action on the uterine muscle in vitro, one through changes in the membrane activity and the other through dissociation of excitation-contraction coupling.

Assessment of myoelectrical signal parameters in estrogen, progesterone, and human chorionic gonadotropin administered in nonpregnant rat myometrium after ovariectomy

“…Estrogen also inhibits Ca 2þ entry (27,28) and K þ channels in smooth-muscle cells from pregnant rat myometrium (29). These findings validate the results of the present study.…”

Long-Term Observations of Uterine Contractions in Nonpregnant Dogs

“…With regard to the involvement of estrogen and progesterone in spontaneous uterine contractions, it is generally considered that estrogen increases uterine contractility [11,22] whereas progesterone decreases it [2,5,6,11,16,29]. In the present study, however, uterine contractile activity occurred during diestrus, even when the plasma progesterone concentration was elevated markedly; and when the plasma estradiol and progesterone concentrations were low, the uterus was quiescent.…”

“…Furthermore, the methods utilized in most studies on uterine contractile activity were measurement of the contractile activity of the isolated myometrium in vitro [1][2][3][4][5][6][7][8] and electromyogram [9][10][11][12][13][14][15] and intrauterine pressure [16][17][18][19][20][21][22] recording in vivo. Although removal of the tissue from its natural environment and elimination of the numerous complex interactions make it easy to perform experiments and understand the underlying mechanisms, in vitro experiments have considerable limitations with respect to understanding the overall picture of uterine contractile activity control.…”

Uterine Contractility in the Nonpregnant Mouse: Changes During the Estrous Cycle and Effects of Chloride Channel Blockade1

“…Spontaneous contractility of the cycling non-pregnant uterus has also been studied in the rat [40][41][42][43], guinea pig [44], dog [45], cow [46][47][48][49] and horse [50,51]. We have revealed that despite considerable variability in contractile behaviors, there are certain motility patterns that are more prevalent at each phase of the cycle; changes which likely correspond to the cyclic variation in the levels and receptor expression of ovarian steroid hormones, estrogen and progesterone, which have been shown to modulate spontaneous contractility in vitro [52][53][54][55][56] and in vivo [41][42][43]57]. Contractions predominately initiated from the oviduct end suggesting this was the dominant pacemaking site, as has been reported by others [41].…”