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Division of Pulmonary and Critical Care Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21224
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 µm 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
PO2 of 2 mmHg; half-maximal at
PO2 of 40 mmHg; blocked by exposure to
Ca2+-free conditions, nifedipine, or ryanodine; and absent
in E+ bronchial arteries of similar size. Hypoxic constrictions were
unaltered by indomethacin, enhanced by indomethacin plus
NG-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.
vascular smooth muscle; internal diameter; calcium; acetylcholine; U-46619; potassium chloride
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