Endothelium dependence of prostanoid-induced relaxation in human hand veins

The endothelium dependence of prostanoid-induced relaxation was examined in human isolated hand veins precontracted by endothelin. Indomethacin (10^-6 mol l^-1) and the thromboxane A₂-receptor antagonist BM 13.505 (10^-6 mol l^-1) were present throughout. The endothelium was removed by insufflating carbogen through the vessel lumen. Prostaglandin (PG) F_2α, PGE₁ PGE₂, and prostacyclin (PGI₂) elicited concentration-dependent relaxant effects. Removal of the endothelium reduced the relaxation induced by PGE_2α and PGE₂, but not that elicited by PGE₁ and PGI₂. The order of potency was PGE₂? PGE₁? PGI₂? PGF_2α regardless of the presence or absence of endothelium. The relaxation elicited by an acidified solution of NaNO₂ (generating nitric oxide) was almost identical in intact and endothelium-denuded vein segments. The results are compatible with the existence of two prostanoid receptor populations mediating relaxation: (1) one located on the smooth muscle cells and; (2) another present on the endothelium or possibly on the smooth muscle and modulated by the endothelium. The latter receptor appears to be activated by PGF_2α and PGE₂, but not by PGE₁ and PGI₂.