Control of myometrial function in preterm versus term labor.
In this review I have attempted to briefly describe myogenic, neurogenic, and hormonal mechanisms which control myometrial function during term and preterm labor. The synthesis of myometrial gap junctions and receptors in response to hormonal changes appears to be a key element in the gradual evolution of contractility leading to labor. I suggest that the development of myometrial gap junctions is physiologically regulated and can be manipulated pharmacologically. Thus, this system provides a means of regulating myogenic control of smooth muscle. I have proposed a model, or working hypothesis, which may explain the indirect and direct interactions of various substances involved in the control of synthetic processes and stimulating or inhibiting myometrial contractility. The model predicts that term or preterm labor can be initiated at various steps. A more complete understanding of these interactions is necessary for a rational approach to the control of term or preterm labor.
D004594:Electrophysiology; D004958:Estradiol / Q000502:physiology; D005260:Female; D006801:Humans; D007365:Intercellular Junctions / Q000502:physiology / Q000648:ultrastructure; D007743:Labor, Obstetric; D008954:Models, Biological; D009215:Myometrium / Q000502:physiology* / Q000503:physiopathology / Q000648:ultrastructure; D007752:Obstetric Labor, Premature / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011374:Progesterone / Q000502:physiology; D011453:Prostaglandins / Q000502:physiology; D012065:Relaxin / Q000502:physiology; D014590:Uterine Contraction; D014599:Uterus / Q000294:innervation
D011453:Prostaglandins; D011374:Progesterone; D004958:Estradiol; D012065:Relaxin