Graded response of K+ current, membrane potential, and [Ca2+]i to hypoxia in pulmonary arterial smooth muscle

Andrea Olschewski, Zhigang Hong, Daniel P. Nelson, E. Kenneth Weir

Research output: Contribution to journalArticlepeer-review

51 Scopus citations


Many studies indicate that hypoxic inhibition of some K+ channels in the membrane of the pulmonary arterial smooth muscle cells (PASMCs) plays a part in initiating hypoxic pulmonary vasoconstriction. The sensitivity of the K+ current (Ik), resting membrane potential (Em), and intracellular Ca2+ concentration ([Ca2+]i) of PASMCs to different levels of hypoxia in these cells has not been explored fully. Reducing PO2 levels gradually inhibited steady-state Ik of rat resistance PASMCs and depolarized the cell membrane. The block of Ik by hypoxia was voltage dependent in that low O2 tensions (3 and 0% O2) inhibited Ik more at 0 and -20 mV than at 50 mV. As expected, the hypoxia-sensitive Ik was also 4-aminopyridine sensitive. Fura 2-loaded PASMCs showed a graded increase in [Ca2+]i as PO2 levels declined. This increase was reduced markedly by nifedipine and removal of extracellular Ca2+. We conclude that, as in the carotid body type I cells, PC-12 pheochromocytoma cells, and cortical neurons, increasing severity of hypoxia causes a proportional decrease in Ik and Em and an increase of [Ca2+]i.

Original languageEnglish (US)
Pages (from-to)L1143-L1150
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number5 27-5
StatePublished - Nov 1 2002
Externally publishedYes


  • Electrophysiology
  • Hypoxic pulmonary vasoconstriction
  • Ion channels
  • Oxygen
  • Patch clamp


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