Mechanism of Mastoparan-Induced EDRF Release from Pulmonary Artery Endothelial Cells

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Abstract
Mastoparan is a wasp venom peptide that activates G-proteins, certain classes of which are involved in the release of endothelium-derived relaxing factor (EDRF). In the present study, we investigated whether this peptide might be a useful tool with which to elucidate the signal transduction pathways responsible for EDRF release from pulmonary artery endothelium. Mastoparan (10-50 µg/ml) elicited an increase in endothelial cell cytosolic free calcium concentration ([Ca2+]i) and EDRF release in a concentration-dependent manner. Both effects were dependent on Ca2+ influx, as they were inhibited by removal of extracellular Ca2+. In addition, when endothelial cells were suspended in Ca2+-free buffer, mastoparan inhibited ATP-induced increases in [Ca2+]i, presumably by depleting intracellular Ca2+ stores. More importantly, mastoparan also caused the release of fura-2 from dye-loaded endothelial cells, unlike ATP, which did not affect fura-2 loss. These data indicate that although mastoparan may act on G-proteins to elicit release of Ca2+ from intracellular stores, the primary mechanism of action responsible for mastoparan’s ability to elicit EDRF release is an increase in cell membrane permeability followed by an influx of extracellular Ca2+.

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