The physiological basis with uterine myometrium contractions from electro-mechanical/hormonal myofibril function to the term and preterm labor

BACKGROUND: Most labor-related problems can be attributed to the uterine myometrium muscle, as this irritable tissue must suppress its irritability potential during pregnancy. Unfortunately, fewer studies have investigated the causes of this lack of suppression in preterm labor. METHODS: We conducted a scoping narrative review using three online databases (PubMed, Scopus, and Science Direct). RESULTS: The review focused on ion channel functions in the myometrium, including sodium channels [Na K-ATPase, Na-activated K channels (Slo2), voltage-gated (SCN) Na(+), Na(+) leaky channels, nonselective (NALCN) channels], potassium channels [KATP (Kir6) channels, voltage-dependent K channels (Kv4, Kv7, and Kv11), twin-pore domain K channels (TASK, TREK), inward rectifier Kir7.1, Ca(2+)-activated K(+) channels with large (KCNMA1, Slo1), small (KCNN1–3), intermediate (KCNN4) conductance], and calcium channels [L-Type and T-type Ca(2+) channels, calcium-activated chloride channels (CaCC)], as well as hyperpolarization-activated cation channels. These channels' functions are associated with hormonal effects such as oxytocin, estrogen/progesterone, and local prostaglandins. CONCLUSION: Electromechanical/hormonal activity and environmental autocrine factors can serve as the primary practical basis for premature uterine contractions in term/preterm labor. Our findings highlight the significance of. 1. the amplitude rate of hyperpolarization and the frequency of contractions, 2. changes in the estrogen/progesterone ratio, 3. Prostaglandins E/F involvement in initiating potential spikes and the increase of intracytoplasmic Ca(2+). This narrative study highlights the range of hyperpolarization and the frequency of myometrium contractions as crucial factors. The synchronized complex progress of estrogen to progesterone ratio and prostaglandins plays a significant role in initiating potential spikes and increasing intracytoplasmic Ca(2+), which further influences the contraction process during labor. Insights into myometrium physiology gained from this study may pave the way for much-needed new treatments to reduce problems associated with normal and preterm labor.