Arachidonic Acid Inhibits Cysteinyl-Leukotriene Receptor Activation in Human Pulmonary Vessels
There are a few reports suggesting that arachidonic acid may have direct regulatory actions in cells or tissues which are independent of the released endogenous metabolites. Brotherton and co-workers  reported that endothelial cells in culture which released prostacyclin in the presence of arachidonic acid became refractory subsequent to a second stimulation, that is, the cells failed to release significant levels of prostacyclin when compared with the initial challenge. These observations were also supported by the work of Revtyak and co-workers  who demonstrated that both histamine- and A23187-induced prostacyclin release was inhibited in human endothelial cells subsequent to arachidonic acid exposure. These results suggested that arachidonic acid may play a direct regulatory role via interaction with cell surface receptors. The aim of this investigation was to examine the effects of arachidonic acid on human pulmonary arteries and veins by measuring the release of several metabolites subsequent to the arachidonic acid exposure and evaluate the effects of cysteinyl-leukotrienes on this release.
KeywordsTyrosine Histamine Prostaglandin Cytosol Thrombin
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