{'fraction_non_alphanumeric': 0.03554868624420402, 'fraction_numerical': 0.025502318392581144, 'mean_word_length': 5.225961538461538, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
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) F2 alpha, PGE1, PGE2, and prostacyclin (PGI2) elicited concentration-dependent relaxant effects. Removal of the endothelium reduced the relaxation induced by PGF2 alpha and PGE2, but not that elicited by PGE1 and PGI2. The order of potency was PGE2 approximately PGE1 approximately PGI2 > PGF2 alpha 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 PGF2 alpha and PGE2, but not by PGE1 and PGI2.