This review concerns the influence of ovarian steroids and of pregnancy on norepinephrine (NE) metabolism in the adrenergic neurons of the female reproductive tract and speculates on the physiological consequences of this influence. Estrogen and progesterone affect not only the NE content of these nerves but also the turnover of NE, the activity of its synthetic enzyme, and releases of NE from nerve terminals. During pregnancy additional factors including stretch-induced hypertrophy come into play and cause degeneration of the nerves in the uterine corpus. This degeneration makes the muscle supersensitive to NE and may also induce morphological changes in the muscle cell membrane. As a result there may be a withdrawal of neural inhibitory influences on the corpus, allowing spontaneous myogenic contractions to intensify. Although the physiological significance of the steroid-transmitter interactions are still unclear, these nerves per se are of interest because they represent a model system for the study of neuroendocrine regulation in the peripheral nervous system.

No abstract

Ovariectomized white rats were treated as follows: group 1, 6.0 µg estradiol benzoate daily for 5 days; group 2, 6.0 µg estradiol for 3 days, then 1.6 µg estradiol plus 12 mg progesterone for 5 days; group 3, untreated controls. Membrane potentials were recorded from single uterine fibers, tension from the entire uterus. Untreated control fibers were quiescent, having a mean resting potential of 35.2 mv. Estrogen-dominated fibers were rhythmically contractile and had a mean resting potential of 57.6 mv. A train of action potentials accompanied and preceded each contraction of the muscle. In certain areas the fibers showed pacemaker-like characteristics, i.e. slow membrane depolarization between action potentials. Progesterone-dominated fibers had significantly higher resting potentials, mean 63.8 mv, but no localized pacemaker areas. Action potentials did not consistently precede or accompany contractions. In groups 1 and 2, acetylcholine stimulated contractions, lowered the membrane potential and increased the discharge rate of action potentials. Epinephrine diminished contractions, raised the membrane potential and abolished the action potential discharge.

This study compares the effects of two inhibitors of prostaglandin synthesis, indomethacin and aspirin, on the longitudinal muscle (LM) and circular muscle (CM) of the rat uterus.