Endothelin induces the Ca(2+)-transient in endothelial cells in situ.

Using front-surface fluorometry of fura-2 and valvular strips of the pig aorta, we recorded changes in the cytosolic Ca2+ concentration, Ca2+]i, of endothelial cells in situ, quantitatively, and investigated the effects of endothelin-1 and -3 on these endothelial cells. Both endothelin-1 and -3 elevated Ca2+]i of a peak (the first phase) and sustained type. This first phase is considered to be due to a release of Ca2+ from intracellular storage sites. The sustained phase depended on extracellular Ca2+ and is considered to be due to an influx of Ca2+ through the plasma membrane. At equimolar concentrations, the peak elevations of Ca2+]i induced by endothelin-1 were much higher than those induced by endothelin-3. We suggest that, in endothelial cells in situ, endothelin-1 mobilizes stored Ca2+ and may activate Ca(2+)-sensitive pathways, including the release of prostacyclin and endothelium-derived relaxing factors, more potently than does endothelin-3.