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Journal of Endocrinology (1992) 132, 77-82       DOI: 10.1677/joe.0.1320077
© 1992 Society for Endocrinology
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Arachidonic acid-induced LH release is ATP-independent and insensitive to N-ethyl maleimide

P. V. Kaye, P. A. van der Merwe, R. P. Millar and J. S. Davidson

The mechanism of arachidonic acid (AA)-induced LH release was characterized using sheep pituitary cells in primary culture permeabilized with Staphylococcal {alpha}-toxin. In intact cells, exogenous AA evoked release of LH in a manner which was partially dependent on extracellular Ca2+. At similar concentrations, AA also caused cell permeabilization as monitored by efflux of [3H]2-deoxyglucose metabolites. In {alpha}-toxin-permeabilized cells where cytosolic Ca2+ was clamped at resting levels, AA retained its ability to cause LH release. Unlike the stimulation of exocytosis produced by Ca2+, phorbol ester or cyclic AMP, AA-evoked release was independent of ATP and was not inhibited by pretreatment with N-ethyl maleimide. These findings indicated that exogenous AA does not cause LH release by Ca2+ influx or mobilization or by activating protein kinase C. The results suggest that LH release induced by exogenous AA is probably due to its detergent-like properties, and does not represent true exocytosis.

Journal of Endocrinology (1992) 132, 77–82




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