
Leukotriene C promotes prostacyclin synthesis by human endothelial cells.
Author(s) -
Eva B. Cramer,
Laura G. Pologe,
Nicholas A. Pawlowski,
Zanvil A. Cohn,
William Scott
Publication year - 1983
Publication title -
proceedings of the national academy of sciences of the united states of america
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.011
H-Index - 771
eISSN - 1091-6490
pISSN - 0027-8424
DOI - 10.1073/pnas.80.13.4109
Subject(s) - prostacyclin , arachidonic acid , leukotriene , umbilical vein , leukotriene c4 , chemistry , metabolite , leukotriene b4 , phosphatidylethanolamine , prostaglandin , lipoxygenase , biochemistry , vasodilation , phosphatidylcholine , pharmacology , medicine , endocrinology , biology , phospholipid , enzyme , in vitro , inflammation , membrane , asthma
Cultured endothelial cells from human umbilical vein were labelled with [3H]arachidonic acid for 16 hr. The radiolabel was localized primarily in phospholipids (93%) and 73% was distributed equally between phosphatidylcholine and phosphatidylethanolamine. Leukotriene C (10-1,000 nM) promoted a dose-dependent release of radiolabel into the culture medium. This response was 3.3 times control values at 100 nM. The major arachidonic acid metabolite synthesized was prostacyclin, which was 33% of the total released radiolabel. Endothelial cells also released small amounts of prostaglandin F2 alpha (6.1%), unidentified lipoxygenase products (14.8%), and unreacted arachidonic acid (33%). The 30-min time course of release was independent of the leukotriene C concentration used. Leukotriene D at similar concentrations also promoted endothelial cells to release primarily prostacyclin and unreacted arachidonic acid. The release of prostacyclin, a potent vasodilator agent, may be an important mediator in slow reacting substance effects on the vasculature.