The physiological basis with uterine myometrium contractions from electro-mechanical/hormonal myofibril function to the term and preterm labor
Farideh Zafari Zangeneh, Sedighe Hantoushzadeh
Abstract
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.