Mechanisms of hypoxic vasodilation in ferret pulmonary arteries

C. M. Wiener, M. R. Banta, M. S. Dowless, N. A. Flavahan, J. T. Sylvester

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To investigate the mechanism of hypoxic pulmonary vasodilation we measured isometric tension in rings from ferret third- to fifth-generation intrapulmonary arteries mounted in organ baths (37°C, 28% O2-5% CO2). After precontraction with phenylephrine (PE), hypoxia caused a brief transient vasoconstriction followed by marked vasodilation. Endothelial denudation did not affect the steady-state response. In vessels without endothelium, inhibition of cyclooxygenase and nitric oxide synthase had no effect on the response to hypoxia. Inhibition of ATP-dependent K+ channels (K(ATP)) with glibenclamide, linogliride, or tolbutamide had no effect on normoxic tone before PE or the vasoconstrictor response to PE but inhibited hypoxic vasodilation. Inhibition of Ca2+-activated K+ (K(Ca)) channels with charybdotoxin potentiated the vasoconstrictor response to PE but had no effect on hypoxic vasodilation. The nonspecific K+-channel inhibitor tetraethylammonium (TEA) potentiated the response to PE and inhibited hypoxic vasodilation. Glibenclamide plus TEA inhibited hypoxic vasodilation more than either agent alone, suggesting that TEA inhibited the K(ATP)-channel independent vasodilation. These results suggest that in isolated ferret pulmonary arteries hypoxia causes vasodilation partially by activating smooth muscle K(ATP) channels. Activation of a TEA-sensitive channel that is not a K(ATP) or K(Ca) channel may also contribute to hypoxic vasodilation.

Original languageEnglish (US)
Pages (from-to)L351-L357
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number3 13-3
StatePublished - Oct 13 1995


  • charybdotoxin
  • glibenclamide
  • linogliride
  • pulmon ary vascular resistance
  • tetraethylammonium
  • tolbutamide

ASJC Scopus subject areas

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


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