K+ is the major ion responsible for such changes in ion flux, reflecting changes in various K+ channels. Excitation-contraction
As the uterus becomes essentially denervated during gestation, it is unlikely that any coordinated nervous regulation of the myometrium is centrally orchestrated. Excitation
The excitation-contraction coupling of uterine smooth muscle is also very similar to that of other smooth muscle in general, with intracellular increase in calcium (Ca2+) leading to contraction. Nitric oxide (NO) is particularly effective in relaxing the myometrium and in fact has a lower inhibitory concentration 50% (Ki) in human than guinea pig or non-human primate myometrium. Restoration to resting state
Uterine smooth muscle mechanisms of relaxation differ significantly from those of other human smooth muscles. Removal of Ca2+ after contraction induces relaxation of the smooth muscle, and restores the molecular structure of the sarcoplasmic reticulum for the next contractile stimulus. Measuring uterine contractility ex vivo
Ethically-donated human uterine tissues can be used to measure uterine contractility ex vivo. In these experiments, sections of myometrium are set up in an organ bath system that to measure changes in isometric force production. Following functional checks to ensure the tissue is physiologically active, compounds can be added to the organ bath in increasing concentrations to create a cumulative concentration-response curve (CCRC).A key advantage of measuring uterine contractility ex vivo is the ability to eliminate species differences. For example, while magnesium reduces myometrial contractility in animal studies and in vitro, it does not demonstrate the same effect in clinical studies.
This change typically occurs at night, suggesting neural control, and significantly increases intrauterine pressure. Some women may experience contractions before labour is due. These are Braxton Hicks contractions, which are sometimes referred to as "false labour." There are several endogenous compounds involved in coordinating uterine contractility in labour, including oxytocin and prostaglandins. Oxytocin
The hormone oxytocin has been identified as inducing uterine contractions, and labour in general. Oxytocin is produced by the body naturally and since the 1950s has also been available in synthetic pharmaceutical form. In either form, oxytocin stimulates uterine contractions to accelerate the process of childbirth. Production and secretion of oxytocin is controlled by a positive feedback mechanism, where its initial release, either naturally or in pharmaceutical form, stimulates production and release of further oxytocin. For example, when oxytocin is released during a contraction of the uterus at the start of childbirth, this stimulates production and release of more oxytocin and an increase in the duration, intensity and frequency of contractions. This process compounds in intensity and frequency and continues until the triggering activity ceases. Prostaglandins
The concentration of prostaglandins in the blood plasma and amniotic fluid increases during labor. These inflammatory mediators encourage myometrial contractions to induce labor. Prostaglandins are also related to the changes in gap junction formation and connexin-43 expression during labor. In orgasm
Uterine and vaginal contractions usually take place during female sexual stimulation, including sexual arousal, and orgasm.