A biochemical hypothesis to explain the mechanism of luteal regression

It seems likely that luteal regression may involve a direct biochemical action of prostaglandin F2alpha (PGF2alpha) on the luteal cell since there are now several reports that PGF2alpha can directly inhibit steroidogenesis in vitro. However, the mechanism of such an action of PGF2alpha remains obscure. This article initially reviews the central role of adenosine 3,I5I-mono-phosphate (c-AMP) in initiating and maintaining the structural and functional changes occurring on luteinisation. A mechanism is suggested, supported by results obtained using granulosa cells in tissue culture, in which PGF2alpha initiates functional luteolysis by inhibiting further synthesis of c-AMP. This mechanism is then used in conjunction with further in vitro observations to provide a possible explanation for the inability of PGF2alpha to regress newly formed corpora lutea. Finally, the possible mechanisms of structural regression are discussed.