Prostacyclin (PGI2),
thromboxane A2 (TXA2) and
F2-isoprostanes,
prostaglandin F2-like compounds, have wide and contrasting spectrum of
biological activities and may influence blood pressure and
atherogenesis. To investigate the dynamics of PGI2, TXA2 and
F2-isoprostanes in patients with
hypertension and
hyperlipidemia (HH group), we measured the major urinary metabolites of PGI2: 6-keto
PGF1alpha (Keto) and 2,3-dinor-6-keto
PGF1alpha, (
Dinor), those of TXA2:TXB2 and 11-dehydro TXB2 (Dehydro), and urinary
8-isoprostane (Iso) in 34 patients. Urinary excretion of
Dinor was significantly lower in patients than in controls and that of Dehydro was significantly higher in patients than in controls. Keto, TXB2 and Iso were not significantly different between them.
Antiplatelet agents decreased not only TXA2 metabolites but also PGI2 metabolites. Urinary
C-peptide immunoreactivity was correlated with
Dinor and Dehydro. After administration of
eicosapentaenoic acid (EPA), total
cholesterol (T-cho) and
triglycerides (TG) significantly decreased. Although
prostanoids did not show significant change, changes in T-cho were correlated with changes in
Dinor and changes in Iso. These results suggest that PGI2 and TXA2 of systemic origin might be related to the pathophysiology of
hypertension and
hyperlipidemia and that the dynamics of PGI2, TXA2 and
F2-isoprostanes might be related to not only blood pressure regulation but also
lipid and
glucose metabolism.