Changes in prostacyclin, thromboxane A2 and F2-isoprostanes, and influence of eicosapentaenoic acid and antiplatelet agents in patients with hypertension and hyperlipidemia

Prostacyclin (PGI(2)), thromboxane A(2) (TXA(2)) and F-2-isoprostanes, prostaglandin F-2-like compounds, have wide and contrasting spectrum of biological activities and may influence blood pressure and atherogenesis. To investigate the dynamics of PGI(2), TXA(2) and F-2-isoprostanes in patients with hypertension and hyperlipidemia (HH group), we measured the major urinary metabolites of PGI(2): 6-keto PGF(1 alpha) (Keto) and 2,3-dinor-6-keto PGF(1 alpha) (Dinor), those of TXA(2): TXB2 and 11-dehydro TXB2 (Dehydro), and urinary 8-isoprostane (Iso) in 34 patients. Urinary excretion of Diner 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 TXA(2) metabolites but also PGI(2) metabolites. Urinary C-peptide immunoreactivity was correlated with Diner 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 Diner and changes in Iso. These results suggest that PGI(2) and TXA(2) of systemic origin might be related to the pathophysiology of hypertension and hyperlipidemia and that the dynamics of PGI(2), TXA(2) and F-2-isoprostanes might be related to not only blood pressure regulation but also lipid and glucose metabolism. (C) 1999 Elsevier Science B.V. All rights reserved.