Tutoring at home

Myometrial cells have developed a unique system of regulatory pathways that rely not only on estrogen and progesterone receptors but also on a variety of cell surface receptors that can directly regulate the contractile state of the cell. The three major classes of cell surface receptors are the G-protein–linked, ion channel–linked, and enzyme-linked. Multiple examples of each class of receptors have been identified in human myometrium, and examples of each class appear to be modified during the phases of parturition. Most of these heptahelical receptors are associated with the activation of adenylyl cyclase. Other heptahelical receptors in myometrium, however, are more commonly associated with G-protein–mediated activation of phospholipase C, which will lead to increased [Ca2+]i and myometrial cell contraction. Many G-protein–coupled receptors that participate in regulation of myometrial activity have been characterized. These were reviewed recently by Lopez (2003).
Ligands for the heptahelical receptors include neuropeptides, hormones, and autacoids. Many of these are available to the myometrium during pregnancy in high concentration by several routes: from maternal blood (endocrine), contiguous tissues or adjacent cells (paracrine), or direct synthesis in the myometrial smooth muscle cells (autocrine) (Fig. 6–16). It is important to note that the myometrial response to a hormone can change during the course of pregnancy. Thus, it is conceivable that hormone action on the myometrium is regulated at several levels, including the expression of the heptahelical receptor, its associated G-proteins, or the effector proteins in the plasma membrane. Specifically, the imposition of quiescence (activation of adenylyl cyclase) or the facilitation of contractions (activation of phospholipase C and increased [Ca2+]i) may in some cases be regulated by the same hormone.