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- W2113158482 abstract "To determine the role of endothelium in hypoxic pulmonary vasoconstriction (HPV), we measured vasomotor responses to hypoxia in isolated seventh-generation porcine pulmonary arteries < 300 microm in diameter with (E+) and without endothelium. In E+ pulmonary arteries, hypoxia decreased the vascular intraluminal diameter measured at a constant transmural pressure. These constrictions were complete in 30-40 min; maximum at PO(2) of 2 mm Hg; half-maximal at PO(2) of 40 mm Hg; blocked by exposure to Ca(2+)-free conditions, nifedipine, or ryanodine; and absent in E+ bronchial arteries of similar size. Hypoxic constrictions were unaltered by indomethacin, enhanced by indomethacin plus N(G)-nitro-L-arginine methyl ester, abolished by BQ-123 or endothelial denudation, and restored in endothelium-denuded pulmonary arteries pretreated with 10(-10) M endothelin-1 (ET-1). Given previous demonstrations that hypoxia caused contractions in isolated pulmonary arterial myocytes and that ET-1 receptor antagonists inhibited HPV in intact animals, our results suggest that full in vivo expression of HPV requires basal release of ET-1 from the endothelium to facilitate mechanisms of hypoxic reactivity in pulmonary arterial smooth muscle." @default.
- W2113158482 created "2016-06-24" @default.
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- W2113158482 date "2001-05-01" @default.
- W2113158482 modified "2023-09-25" @default.
- W2113158482 title "Hypoxic constriction of porcine distal pulmonary arteries: endothelium and endothelin dependence" @default.
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- W2113158482 doi "https://doi.org/10.1152/ajplung.2001.280.5.l856" @default.
- W2113158482 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/11290508" @default.
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