Beschreibung:
<jats:p> The main aim of this study was to determine the effects of endothelium removal on tension and intracellular Ca<jats:sup>2+</jats:sup>([Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>) during hypoxic pulmonary vasoconstriction (HPV) in rat isolated intrapulmonary arteries (IPA). Rat IPA and mesenteric arteries (MA) were mounted on myographs and loaded with the Ca<jats:sup>2+</jats:sup>-sensitive fluorophore fura PE-3. Arteries were precontracted with prostaglandin F<jats:sub>2α</jats:sub>, and the effects of hypoxia were examined. HPV in isolated IPA consisted of a transient constriction superimposed on a second sustained phase. Only the latter phase was abolished by endothelial denudation. However, removal of the endothelium had no effect on [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> at any point during HPV. The endothelin-1 antagonists BQ-123 and BQ-788 did not affect HPV, although constriction induced by 100 nM endothelin-1 was abolished. In MA, hypoxia induced an initial transient rise in tension and [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub>, followed by vasodilatation and a fall in [Ca<jats:sup>2+</jats:sup>]<jats:sub>i</jats:sub> to (but not below) prehypoxic levels. These results are consistent with sustained HPV being mediated by an endothelium-derived constrictor factor that is distinct from endothelin-1 and that elicits vasoconstriction via Ca<jats:sup>2+</jats:sup>sensitization. </jats:p>