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

Q. Liu, J. S.K. Sham, L. A. Shimoda, J. T. Sylvester

Research output: Contribution to journalReview articlepeer-review

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 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.

Original languageEnglish (US)
Pages (from-to)L856-L865
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume280
Issue number5 25-5
DOIs
StatePublished - May 2001

Keywords

  • Acetylcholine
  • Calcium
  • Internal diameter
  • Potassium chloride
  • U-46619
  • Vascular smooth muscle

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology

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