The requirement of extra and/or in-tracellular CQ++ to stimulate prosta-glandins synthesis varies in different tissues . Poyser, (1985), elicited that prosta-gtandins synthesis and efflux from their active biosynthetic sites in almost tissues is dependent upon mobiliza­tion of Ca++ from intracellular stores. The extracellular Ca++ is essential for release of Ca++ from intracellular stores and essential for replenish these stores., Rilley & Poyser, (1987).
Ernest et al.. (1983), reported that the activity of phospholipase seems to be increased by the presence of Ca⁺⁺. PLA2 is extremly important in the re­lease of arachidontc acid, (which is the most abundent of prostaglandins precursors in almost all the tissues), followed by a rise of prostaglandins bi­osynthesis. So PLA2 is considered as
a regulating and triggering enzyme for prostaglandins biosynthesis.
Prostagiadins are not stored pre­formed but are synthesized and re­leased as required. Therefore the in­creased efflux reflects the increased biosynthesis and not release of prost-glandins as endogenous constituents Ramwell & Shaw, 1970 and Olley & Coceani, (1980).
Synthesis of PGF2 & may be derived from PGE2 and/or from PGD2. The in-terconversion between PGF2 & and PGFg is dought, Yamamoto, (1983), reported that there is no a direct inter-conversion between PGE2 and PGF2 &. In contrast Ernest et al., (1983) found that reduction of the Ketogroup at Cg in PGE2 to form PGF2 & com­pound is found to take place in guinea pig as weil as in human.