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


      Journal of Vascular Research

      S. Karger AG

      Endothelium, Nitric oxide, EDRF, Mastoparan, Calcium, Pulmonary

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          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 ([Ca<sup>2+</sup>]<sub>i</sub>) and EDRF release in a concentration-dependent manner. Both effects were dependent on Ca<sup>2+</sup> influx, as they were inhibited by removal of extracellular Ca<sup>2+</sup>. In addition, when endothelial cells were suspended in Ca<sup>2+</sup>-free buffer, mastoparan inhibited ATP-induced increases in [Ca<sup>2+</sup>]<sub>i</sub>, presumably by depleting intracellular Ca<sup>2+</sup> 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 Ca<sup>2+</sup> 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 Ca<sup>2+</sup>.

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          Author and article information

          J Vasc Res
          Journal of Vascular Research
          S. Karger AG
          23 September 2008
          : 30
          : 2
          : 68-72
          Department of Pharmacology, University of Virginia Health Sciences Center, Charlottesville, Va., USA
          158977 J Vasc Res 1993;30:68–72
          © 1993 S. Karger AG, Basel

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          Page count
          Pages: 5
          Research Paper


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