Point:Counterpoint "Release of an endothelium-derived vasoconstrictor and RhoA/Rho kinase-mediated calcium sensitization of smooth muscle cell contraction are/are not the main effectors for full and sustained hypoxic pulmonary vasoconstriction"

J Appl Physiol (1985). 2007 May;102(5):2077-8; discussion 2080. doi: 10.1152/japplphysiol.01435.2006.
No abstract available

Publication types

  • Letter
  • Comment

MeSH terms

  • Animals
  • Calcium / metabolism
  • Calcium Signaling*
  • Endothelin-1 / metabolism
  • Endothelins / metabolism*
  • Endothelium, Vascular / metabolism
  • Humans
  • Hypoxia / metabolism*
  • Hypoxia / physiopathology
  • Intracellular Signaling Peptides and Proteins / metabolism*
  • Muscle, Smooth, Vascular / metabolism
  • Potassium Channels, Voltage-Gated / metabolism
  • Protein Serine-Threonine Kinases / metabolism*
  • Pulmonary Artery / enzymology
  • Pulmonary Artery / metabolism*
  • Vasoconstriction*
  • rho-Associated Kinases
  • rhoA GTP-Binding Protein / metabolism*

Substances

  • Endothelin-1
  • Endothelins
  • Intracellular Signaling Peptides and Proteins
  • Potassium Channels, Voltage-Gated
  • Protein Serine-Threonine Kinases
  • rho-Associated Kinases
  • rhoA GTP-Binding Protein
  • Calcium