Activity of platelet-activating-factor-acetylhydrolase and the nitric oxide metabolite level in the plasma of pregnant women who develop transient hypertension during later pregnancy.

It is reported that plasma platelet-activating-factor-acetylhydrolase (PAF-AH) is elevated in patients with essential hypertension. In this study, plasma PAF-AH activity was measured during pregnancy and after delivery to examine the relationship between plasma PAF-AH activity and the development of transient hypertension (TH) during pregnancy. Moreover, in order to examine the involvement of endothelial injury in TH, the plasma level of nitric oxide metabolite (NOx; NO2+NO3) was measured. The plasma PAF-AH activity in 51 pregnant women was consecutively measured in the 1st, 2nd and 3rd trimesters of gestation, and after delivery. Forty-one cases were normal pregnancies and 10 cases were complicated by TH later during pregnancy. The PAF-AH activity in the normal pregnancy group decreased in the 2nd trimester of gestation compared with the 1st trimester, but was elevated in the TH group. The incidence of elevation of PAF-AH in the TH group was significantly (7/10; 70.0%; P<0.01, Chi-squared test) higher than in the normal pregnancy group (9/41; 22.0%). The plasma NOx levels in the 2nd trimester were higher than those in the 1st trimester in both the normotensive and TH group (P<0.05 for both comparisons). The 51 patients were classified into two groups according to the change in the PAF-AH in the 2nd trimester: group A consisted of 35 patients whose PAF-AH activity did not increase, and group B consisted of 16 patients whose PAF-AH activity increased. The incidence of development of TH during later pregnancy in group B was significantly (7/16; 43.8%; P<0.01, Chi-squared test) higher than in group A (3/35; 8.6%). Hypertension developed after 36 weeks' gestation in all patients in the TH group. The results of the present study suggest that changes in PAF metabolism may relate to regulation of blood pressure in pregnant women whose pregnancy is complicated with TH, whereas NO metabolism does not differ between women with TH and those having a normal pregnancy.

Cortisol and TGF-beta inhibit secretion of platelet-activating factor-acetylhydrolase in a monocyte-macrophage model system [corrected].

Recent studies have suggested that platelet activating factor (PAF) plays an important role in various reproductive functions, including ovulation, implantation and parturition, and that the local concentration of PAF is modulated by PAF-acetylhydrolase (PAF-AH), a potent PAF inactivator. In this study, we investigated the possible effects of various bioactive substances, which are present at high concentrations in the human pregnant uterus, on PAF-AH secretion from decidual macrophages using a monocyte-macrophage model system, human myelocytic leukaemia cells (HL-60). By treatment with 12-O-tetradecanoylphorbol-13-acetate (TPA), HL-60 cells were transformed to macrophage-like cells, which secreted PAF-AH into the culture medium time- and dose-dependently. After treatment with 10(-8) M TPA, the effects of various substances on the secretion of PAF-AH were examined. Among the substances examined, cortisol and TGF-beta suppressed PAF-AH secretion from TPA-stimulated HL-60 cells in a significant and dose-dependent way. Endothelin, epidermal growth factor, and brain natriuretic peptide had no significant effect on PAF-AH secretion from TPA-stimulated HL-60 cells. These results suggest that local PAF concentrations in the pregnant uterus might be regulated, at least partly, by cortisol and TGF-beta; thus these substances may play a role in the initiation of parturition via regulation of local PAF concentrations.