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- W2034373437 abstract "The mechanism of Hypoxic Pulmonary Vasoconstriction is unknown. The role of endothelin-1 in hypoxic pulmonary vasoconstriction was studied in precontracted small and large pulmonary arteries using the endothelin ETA receptor antagonist sodium-2-benzol [1,3]dioxol-5-yl-4-(4-methoxyphenyl)-4-oxo-3-(3,4,5-trimethoxy-benzyl)-but-2-enoate (CI-1020). Small rat pulmonary arteries exhibit a mixed endothelin ETA receptor and endothelin ETB2 receptor population whereas large rat pulmonary arteries contain only endothelin ETA receptors. CI-1020 inhibited endothelin-1 in small vessels via endothelin ETA receptor blockade (1 and 10 μM) and at high concentrations via endothelin ETA receptor and endothelin ETB2 receptor blockade (100 μM). CI-1020 (0.01, 0.1 and 1 μM) inhibited endothelin-1 in large vessels via endothelin ETA receptor blockade alone. CI-1020 (1, 10 and 100 μM) significantly reduced hypoxic pulmonary vasoconstriction in small vessels, by −9.8±1.4, −9.2±2.3 and −8.0±1.7% 80 mM K+, respectively, compared to +2.5±4.2% with vehicle (P<0.05). CI-1020 (0.01, 0.1 and 1 μM) had no significant effect upon hypoxic pulmonary vasoconstriction in large vessels. In small, but not large, pulmonary arteries hypoxic pulmonary vasoconstriction is due in part to the action of endothelin-1 at the endothelin ETA receptor." @default.
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- W2034373437 date "1999-06-01" @default.
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- W2034373437 title "The effect of the endothelin ETA receptor antagonist CI-1020 on hypoxic pulmonary vasoconstriction" @default.
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- W2034373437 doi "https://doi.org/10.1016/s0014-2999(99)00300-3" @default.
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