Ciliary beat frequency controlled by oestradiol and progesterone during ovarian cycle in guinea-pig Fallopian tube.

The ciliary beat frequency (CBF) of guinea-pig fimbria during the ovarian cycle was measured by video microscopy using a high-speed camera (500 Hz). In the follicular phase, with increasing concentrations of beta-oestradiol ([beta E(2)]) and a low concentration of progesterone ([PRG]), CBF increased from 13.5 to 16 Hz. In the ovulatory phase, with further increase of [beta E(2)], CBF decreased gradually from 16 to 13.5 Hz. In the early luteal phase, with low [PRG] and [beta E(2)], CBF increased to similar to 17 Hz; however, in the middle luteal phase, with increasing [PRG], CBF decreased (similar to 12 Hz), and in the late luteal phase, with decreasing [PRG], CBF increased to similar to 15 Hz. Then, in the resting phase, with low [beta E(2)] and [PRG], CBF decreased immediately to similar to 14 Hz. The CBF of the fimbria was measured in guinea-pigs treated with beta-oestradiol benzoate (beta E(2)B) or medroxyprogesterone (mPRG). A low dose of beta E(2)B increased CBF to similar to 14.5 Hz, whereas a high dose decreased it to similar to 11 Hz. A beta E(2) receptor blocker, ICI-182,780, abolished the beta E(2)B-induced CBF changes and maintained CBF at similar to 12.0 Hz. Medroxyprogesterone decreased CBF to similar to 12.5 Hz, and mifepristone (a PRG receptor blocker) abolished the mPRG-induced CBF decrease and maintained CBF at similar to 15 Hz. The addition of both blockers increased CBF to similar to 18 Hz, suggesting that activation of beta E(2) or PRG receptors decreases the CBF of the fimbria. In conclusion, a moderate [beta E(2)] increase maintains a high CBF (15.5 Hz) in the follicular phase, and then further [beta E(2)] increase decreases CBF to 13.5 Hz in the ovulatory phase. In the early and late luteal phase, low [beta E(2)] and [PRG] increase CBF to 17 and 15 Hz, respectively, and in the middle luteal phase a high [PRG] decreases CBF (to similar to 12 Hz). Thus, the CBF of the fimbria was controlled by signals via beta E(2) and PRG receptors in guinea-pigs.