High altitude pulmonary hypertension: Role of K+ and Ca2+ channels

Carmelle V. Remillard, Jason X.J. Yuan

Research output: Contribution to journalReview articlepeer-review

38 Scopus citations


Global alveolar hypoxia, as experienced at high-altitude living, has a serious impact on vascular physiology, particularly on the pulmonary vasculature. The effects of sustained hypoxia on pulmonary arteries include sustained vasoconstriction and enhanced medial hypertrophy. As the major component of the vascular media, pulmonary artery smooth muscle cells (PASMC) are the main effectors of the physiological response(s) induced during or following hypoxic exposure. Endothelial cells, on the other hand, can sense humoral and hemodynamic changes incurred by hypoxia, triggering their production of vasoactive and mitogenic factors that then alter PASMC function and growth. Transmembrane ion flux through channels in the plasma membrane not only modulates excitation-contraction coupling in PASMC, but also regulates cell volume, apoptosis, and proliferation. In this review, we examine the roles of K+ and Ca2+ channels in the pulmonary vasoconstriction and vascular remodeling observed during chronic hypoxia-induced pulmonary hypertension.

Original languageEnglish (US)
Pages (from-to)133-146
Number of pages14
JournalHigh Altitude Medicine and Biology
Issue number2
StatePublished - Jun 2005
Externally publishedYes


  • Chronic hypoxia
  • Ion channels
  • Membrane potential
  • Proliferation
  • Vascular smooth muscle

ASJC Scopus subject areas

  • Physiology
  • Public Health, Environmental and Occupational Health


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