The ventilatory response to hypoxia

Philip J. Berger (), Elizabeth M. Skuza, Vojta Brodecky and Malcolm H. Wilkinson
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Philip J. Berger: Ritchie Centre for Baby Health Research, Monash Institute of Reproduction and Development, Monash Medical Centre
Elizabeth M. Skuza: Ritchie Centre for Baby Health Research, Monash Institute of Reproduction and Development, Monash Medical Centre
Vojta Brodecky: Ritchie Centre for Baby Health Research, Monash Institute of Reproduction and Development, Monash Medical Centre
Malcolm H. Wilkinson: Ritchie Centre for Baby Health Research, Monash Institute of Reproduction and Development, Monash Medical Centre

Nature, 2002, vol. 419, issue 6908, 686-686

Abstract: Abstract Respiratory physiologists traditionally attribute the increased ventilatory response to hypoxia to increased discharge by the carotid-body chemoreceptor, which is transmitted by sensory processes to neurons in the medullary nucleus of the solitary tract1. However, Lipton et al. propose a radically new model2 in which hypoxia causes haemoglobin to release molecules derived from nitric oxide, which then increase ventilation by directly stimulating solitary-tract neurons. Despite the apparent feasibility of this model3,4,5, we show here that the observations of Lipton et al.2 do not invalidate the classic carotid-body-mediated explanation of the hypoxic ventilatory response. We thus question the justification for a new model to account for hypoxia's effect on breathing.

Date: 2002
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DOI: 10.1038/419686a

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