Figure 1.

Schematic diagram showing the major components that control [Ca²⁺]_i in myometrium. These include the contractant hormone pathways that stimulate G-protein coupled (GPCR) and tyrosine kinase (TyKR) receptors, G-proteins composed of Gα subunits (Gα_q, Gα_i and (not shown) Gα_h), the associated Gβ and Gγ subunits, phospholipase C β and γ, which convert PIP₂ to IP₃ and diacylglycerol (DAG). IP₃ binds to IP₃ receptors (IP₃R) in the endoplasmic reticulum (ER), releasing Ca²⁺ from this intracellular store. Another ER release mechanism involves ryanodine receptors (RyR). Other Ca²⁺ entry mechanisms include cation channels responsive to stimuli such as IP₃R activation, DAG and release of Ca²⁺ from the ER (SRCE) and voltage-operated Ca²⁺ channels (VOC). The plasma membrane Ca²⁺ ATPase (PMCA) and the Na/Ca exchanger (NCX) are responsible for moving Ca²⁺ out of the cell; the ER Ca²⁺ ATPase (SERCA) pumps Ca²⁺ back into the ER. There is also a passive leak of Ca²⁺ from the ER. Ca²⁺ has stimulatory effects on the contractile apparatus, resulting in contraction, and also acts as an intracellular signal influencing a number of pathways in the myometrium.