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Intermittent hypoxia: cell to system.

N R Prabhakar1, R D Fields, T Baker

  • 1Department of Physiology and Biophysics, Case Western Reserve University, Cleveland, Ohio 44106, USA. nrp@po.cwru.edu

American Journal of Physiology. Lung Cellular and Molecular Physiology
|August 16, 2001
PubMed
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Intermittent hypoxia impacts cardiorespiratory systems by altering gene expression and carotid body sensitivity. Chronic exposure elevates blood pressure through complex cellular signaling pathways.

Area of Science:

  • Cardiorespiratory Physiology
  • Cellular Mechanisms
  • Neuroscience

Background:

  • Intermittent hypoxia (IH) affects cardiorespiratory systems and cellular mechanisms.
  • Neural impulse activity patterns are critical for gene induction in neuronal cells.
  • Distinct signaling pathways are involved in IH responses.

Purpose of the Study:

  • To present research on the effects of intermittent hypoxia on cardiorespiratory systems and cellular mechanisms.
  • To explore shared and distinct mechanisms underlying different patterns of IH.
  • To investigate the long-term consequences of chronic IH.

Main Methods:

  • Analysis of neural impulse activity patterns.
  • Investigation of carotid body sensitivity to hypoxia.

Related Experiment Videos

  • Assessment of hypoxia-inducible factor-1 (HIF-1) activation.
  • Evaluation of reactive oxygen species (ROS) involvement.
  • Study of serotonin function blockade in the spinal cord.
  • Measurement of respiratory motor output and protein synthesis.
  • Monitoring of arterial blood pressure and associated signaling systems.

    • Main Results:

    • Chronic IH augments carotid body sensitivity and sensory discharge.
    • IH activates HIF-1, with ROS playing a critical role.
    • Serotonin blockade prevents long-term respiratory facilitation, requiring protein synthesis.
    • Chronic IH sustains elevated arterial blood pressure.
    • Associated changes include altered catecholaminergic, renin-angiotensin, and nitric oxide synthase systems.

    Conclusions:

    • Different patterns of IH may share underlying cellular mechanisms.
    • IH significantly impacts carotid body function and neuroplasticity.
    • Chronic IH induces sustained hypertension via neurohumoral pathway alterations.