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Acute reductions in PO2 depolarize pulmonary artery endothelial cells and decrease [Ca2+]i

T Stevens1, D N Cornfield, I F McMurtry

  • 1Department of Medicine, University of Colorado Health Sciences Center, Denver 80262.

The American Journal of Physiology
|April 1, 1994
PubMed
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Acute hypoxia depolarizes pulmonary artery endothelial cells (PAECs), reducing calcium influx and intracellular calcium levels ([Ca2+]i). This study clarifies the immediate impact of low oxygen on PAEC function.

Area of Science:

  • Physiology
  • Cell Biology
  • Cardiovascular Research

Background:

  • Pulmonary artery endothelial cells (PAECs) are sensitive to oxygen levels.
  • The immediate effects of reduced partial pressure of oxygen (PO2) on PAEC membrane potential and intracellular free calcium ([Ca2+]i) were previously unknown.

Purpose of the Study:

  • To investigate the hypothesis that acute hypoxia depolarizes PAECs, inhibits calcium influx, and reduces [Ca2+]i.
  • To elucidate the role of the electrochemical gradient in hypoxia-induced [Ca2+]i reduction.

Main Methods:

  • Utilized fluorescent probes DiBAC4 and fura 2 to measure PAEC membrane potential and [Ca2+]i, respectively.
  • Experimentally decreased PO2 in primary PAEC cultures.
  • Assessed calcium influx via manganese quenching and manipulated extracellular calcium and ion channel activity.

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Main Results:

  • A reduction in PO2 from 125 to 35 mmHg caused significant membrane depolarization.
  • Hypoxia led to a 60% reduction in calcium influx and decreased basal [Ca2+]i from 79 nM to 31 nM.
  • Interventions reducing the electrochemical gradient for calcium entry mimicked the hypoxia-induced [Ca2+]i reduction.

Conclusions:

  • Acute reduction in PO2 directly depolarizes PAECs.
  • Hypoxia inhibits calcium influx and subsequently decreases intracellular calcium levels.
  • The electrochemical gradient plays a crucial role in mediating hypoxia-induced changes in [Ca2+]i.