Figure 7.

Increases in astrocytic [Ca²⁺]_i may lead to GSH-dependent, PgE₂-mediated vasodilation. Schematic diagram depicting how CO₂-evoked increases in astrocytic [Ca²⁺]_i may lead to PgE₂-mediated vasodilation. As a result of elevated [Ca²⁺]_i, PLA₂ is activated. PLA₂ generates AA from the plasma membrane. AA can be processed locally by COX enzymes to produce AA derivatives, such as prostaglandin H₂ (PgH₂). PgE₂ is produced from PgH₂ by the enzyme PGEs, which requires GSH as a cofactor (Jakobsson et al., 1999; Murakami et al., 2000; Tanioka et al., 2000). PgE₂ is released from astrocyte endfeet, which are apposed to the smooth muscle layer surrounding arterioles, resulting in activation of K⁺ channels, a decrease in Ca²⁺ entry into the smooth muscle cell and vasodilation.