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The ventilatory response to hypoxia

Author

Listed:
  • D. Gozal
  • B. M. Gaston

    (University of Virginia School of Medicine)

  • A. J. Lipton
  • M. A. Johnson
  • T. Macdonald
  • M. W. Lieberman

Abstract

We do not challenge the 'classic' theory of peripheral-chemoreceptor-mediated HVR. However, this offers no insight into the mediators of the time-domain components of HVR, such as ventilatory short-term potentiation (VSTP)1. VSTP is critical to respiratory-system stability2 and is unrelated to the activity of the peripheral chemoreceptor3,4, so other factors may have a role in HVR5,6. One such factor involves SNO signalling in brainstem neurons. SNOs could be formed by neuronal nitric oxide synthase (NOS, activated by afferents from peripheral chemoreceptors) and by erythrocyte deoxygenation. Indeed, erythrocyte deoxygenation could be signalled to peripheral chemoreceptors through SNO formation.

Suggested Citation

  • D. Gozal & B. M. Gaston & A. J. Lipton & M. A. Johnson & T. Macdonald & M. W. Lieberman, 2002. "The ventilatory response to hypoxia," Nature, Nature, vol. 419(6908), pages 686-686, October.
    • Handle: RePEc:nat:nature:v:419:y:2002:i:6908:d:10.1038_419686b
    DOI: 10.1038/419686b
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