Evidence for Distinct Endothelin Receptors in the Pulmonary Vascular Bed in vivo

Lippton, Howard; Cohen, Gordon; Knight, Martha; McMurtry, Ivan F.; Gillot, Doug; Arena, Frank; Summer, Warren R.; Hyman, Albert L.

doi:10.1097/00005344-199100177-00105

Cited by 3 publications

(1 citation statement)

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“…ET-induced pulmonary vasoconstriction, unlike HPV, reversed very slowly (4,43), perhaps due to prolonged receptor binding (75). ET-1 caused transient vasodilation during HPV, perhaps by activating K ATP channels in vascular smooth muscle or ET B receptors and NO production in endothelium (10,18,20,(35)(36)(37)80). Some investigators (11,46,51) were unable to demonstrate that hypoxia increased pulmonary ET-1 production.…”

Section: Discussionmentioning

confidence: 99%

Hypoxic constriction of porcine distal pulmonary arteries: endothelium and endothelin dependence

Liu

Sham

Shimoda

et al. 2001

American Journal of Physiology-Lung Cellular and Molecular Phys

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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.

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