1. Dexamethasone was administered to six healthy female volunteers for 4 days, resulting in plasma levels of 4.8 ± 1.4 × 10−8 mol/l. Urinary excretions of six prostanoids as well as collagen-induced platelet thromboxane formation and aggregation were determined before, during and 1 month after administration of dexamethasone.
2. Dexamethasone had no effect on urinary thromboxane B2 (77 ± 22 ng/day vs 63 ± 16 ng/day during dexamethasone), dinor-thromboxane B2, the major urinary metabolite of thromboxane B2 (406 ± 84 ng/day vs 380 ± 90 ng/day), dinor-6-keto-prostaglandin F1α, the major urinary metabolite of prostacyclin (199 ± 41 ng/day vs 237 ± 53 ng/day), tetranor-5,1 l-diketo-7α-hydroxy-prostane-1,16-dioic acid, the major urinary metabolite of prostaglandins E1 and E2 (7712 ± 1677 ng/day vs 7886 ± 2565 ng/day) and tetranor-11-keto-5α, 7α-dihydroxy-prostane-1,16-dioic acid, the major urinary metabolite of prostaglandins F1α and F2α (14 394 ± 2053 ng/day vs 18288 ± 2251 ng/day). Prostaglandin E2 excretion slightly but significantly increased from 217 ± 48 ng/day to 294 ± 55 ng/day. Collagen-induced platelet thromboxane formation and aggregation were not altered.
3. These results suggest that glucocorticoids do not regulate renal, platelet or total body prostanoid formation in healthy man.
