Chronic hypoxia inhibits Kv channel gene expression in rat distal pulmonary artery

Jian Wang, Letitia Weigand, Wenqian Wang, J. T. Sylvester, Larissa A. Shimoda

Research output: Contribution to journalArticlepeer-review


In pulmonary arterial smooth muscle cells (PASMCs), voltage-gated K + (Kv) channels play an important role in regulating membrane potential, cytoplasmic free Ca2+ concentration, and pulmonary vasomotor tone. Previous studies demonstrated that exposure of rats to chronic hypoxia decreased Kv channel function in PASMCs from distal pulmonary arteries (dPA). To determine whether this decrease in function was due to decreased expression of Kv channel proteins and which K v proteins might be involved, we analyzed Kv channel gene expression in intact, endothelium-denuded dPAs obtained from rats exposed to 10% O2 for 3 wk. Kv1.1, KV1.2, KV1.4, Kv1.5, Kv1.6, KV2.1, KV3.1, K V4.3, and KV9.3 channel α-subunits and K v1, KV2, and KV3 β-subunits were expressed in rat dPAs. Exposure to chronic hypoxia decreased mRNA and protein levels of Kv1.1, KV1.5, KV1.6, KV2.1, and KV4.3 α-subunits in dPAs but did not alter gene or protein expression of these channels in aorta. Furthermore, chronic hypoxia did not alter the mRNA levels of β-subunits in dPAs. These results suggest that diminished transcription of Kv α-subunits may reduce the number of functional Kv channels in dPAs during prolonged hypoxia, causing the decreased Kv current previously observed in PASMCs and leading to pulmonary artery vasoconstriction.

Original languageEnglish (US)
Pages (from-to)L1049-L1058
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number6 32-6
StatePublished - Jun 2005


  • Voltage-gated K

ASJC Scopus subject areas

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


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