Octopus vulgaris can regulate its oxygen uptake down to a PO2 of around 6.7 kPa. As the tension falls from 18.6 to 6.7 kPa (140 to 50 mmHg), Pv (the pressure pulse driving the ventilatory flow, measured inside the mantle cavity) can more than double while fv (the ventilation frequency) increases by a few per cent at most. Both changes are reversed when the ambient oxygen tension is returned to normal. Cutting the visceral nerves linking the hearts and gills to the brain prevents these adaptive changes in Pv and fv, as does section of the branchial nerves linking the cardiac ganglia to the gills. Responses to changes in ambient oxygen tension are very fast, beginning within two or three ventilation cycles. It is concluded that changes to Pv and fv depend upon receptors in the gills and on the integrity of a nervous pathway to the brain. Changes in oxygen tension also affect the hearts, where aortic pulse amplitude (Pa) and, to a lesser extent, heartbeat frequency (fh) fall and rise with the ambient PO2. In this case, section of the visceral or branchial nerves has no effect. Responses are again very rapid. It is concluded that the observed fall and return to normoxic values of Pa and fh are local responses to a fall and rise in the oxygen tension of blood coming from the gills into the systemic heart. Changes to ventilation and heartbeat can also occur in normoxic water when oxygen demand rises after feeding. These responses are not prevented by section of the visceral or branchial nerves. Possible control of ventilation and heartbeat through the neurosecretory system in the anterior vena cava is discussed.