Effects of hypoxia in porcine pulmonary arterial myocytes: Roles of K(v) channel and endothelin-1

James S.K. Sham, Benjamin R. Crenshaw, Li Hua Deng, Larissa A. Shimoda, J. T. Sylvester

Research output: Contribution to journalArticlepeer-review

68 Scopus citations


Effects of acute hypoxia on intracellular Ca2+ concentration ([Ca2+](i)) and cell length were recorded simultaneously in proximal and distal pulmonary (PASMCs) and femoral (FASMCs) arterial smooth muscle cells. Reducing Po2 from normoxia to severe hypoxia (Po2 < 10 mmHg) caused small but significant decreases in length and a reversible increase in [Ca2+](i) in distal PASMCs and a small decrease in length in proximal PASMCs but had no effect in FASMCs, even though all three cell types contracted significantly to vasoactive agonists. Inhibition of voltage-dependent K+ (K(v)) channel with 4-aminopyridine produced a greater increase in [Ca2+](i) in distal than in proximal PASMCs. In distal PASMCs, severe hypoxia caused a slight inhibition of K(v) currents; however, it elicited further contraction in the presence of 4-aminopyridine. Endothelin-1 (10-10 M), which itself did not alter cell length or [Ca2+](i), significantly potentiated the hypoxic contraction. These results suggest that hypoxia only has small direct effects on porcine PASMCs. These effects cannot be fully explained by inhibition of K(v) channels and were greatly enhanced via synergistic interactions with the endothelium-derived factor endothelin-1.

Original languageEnglish (US)
Pages (from-to)L262-L272
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number2 23-2
StatePublished - 2000


  • Calcium
  • Pulmonary arterial smooth muscle cell
  • Vasoconstriction
  • Voltage-dependent potassium channel

ASJC Scopus subject areas

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


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