Effects of prostaglandins on cyclic nucleotide phosphodiesterase activity in the human term placenta

Abstract

Slices of human full-term placentas, obtained by elective cesarean section, were incubated in the absence or presence of prostaglandins (PGs) and the cyclic AMP phosphodiesterase (cAMP PDE) activity was measured. PGE 1 and PGI 2 were shown to stimulate cAMP PDE activity. The effect of PGE 1 is related to an increase in the Vmax of the low Km activity without alteration of this apparent Km. Several findings suggest that the cAMP PDE is activated by its own substrate; PGE 1 and PGI 2 promote an increase of cAMP formation which is observed before the cAMP PDE activation. Dibutyryl cAMP or theophylline also activate cAMP PDE. In contrast, PGF 2α does not influence either adenylate cyclase or cAMP PDE. In addition, we found that the ability of the placenta to degrade cAMP, increases after parturition. PG levels are higher in the foeto-placental unit during labor, and a causal relationship between these two phenomena is possible. Our data supporting the concept of hormonal control of cAMP PDE is consistent with the hypothesis that an accelerated cAMP metabolism in placenta contributes to the maintenance of a constant equilibrium of the cyclic nucleotide levels in the foeto-placental unit.