PROSTAGLANDIN-F2-ALPHA-INDUCED ENDOTHELIUM-DEPENDENT RELAXATION IN ISOLATED MONKEY CEREBRAL-ARTERIES

Effects of prostaglandin F2-alpha (PGF2-alpha) on isolated monkey and dog cerebral arteries were investigated to reevaluate PGF2-alpha's possible action on the endothelium. Low concentrations of PGF2-alpha ranging from 10(-11) to 10(-8) M produced a dose-dependent relaxation in the monkey arteries. PGF2-alpha (10(-7) M) produced a transient contraction followed by a small relaxation, whereas higher concentrations (> 10(-6) M) of PGF2-alpha induced only contractions. The PGF2-alpha-induced relaxation was not observed in the canine cerebral arteries. The PGF2-alpha-induced relaxation of the monkey cerebral arteries was not affected by treatment with 10(-7) M propranolol, 10(-7) M atropine, or 10(-6) M cimetidine. In monkey cerebral arteries without endothelium, PGF2-alpha in concentrations ranging from 10(-11) to 10(-6) M caused no relaxation. Treatment with 5 x 10(-5) M aspirin, 3 x 10(-5) M N(G)-monomethyl-L-arginine, and 10(-5) M oxyhemoglobin significantly suppressed the PGF2-alpha-induced relaxation. These results suggest that low concentrations of PGF2-alpha may produce an endothelium-dependent relaxation in monkey cerebral arteries and that the relaxation may be mediated by release of both endogenous vasodilative prostaglandins and endothelium-derived relaxing factor from endothelial cells.