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Brief Communications
Nature 419, 686 (17 October 2002) | doi:10.1038/419686a
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Physiology (communication arising): The ventilatory response to hypoxia
Philip J. Berger, Elizabeth M. Skuza, Vojta Brodecky & Malcolm H. Wilkinson
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.
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