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 model^{3, 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.

1. Ritchie Centre for Baby Health Research, Monash Institute of Reproduction and Development, Monash Medical Centre, Clayton, Victoria 3168, Australia

Correspondence to: e-mail: Email: philip.berger@med.monash.edu.au